Genomes and Genes
Summary: The mitochondria of the myocardium.
Publications305 found, 100 shown here
- Mitochondrial permeability transition pore opening during myocardial reperfusion--a target for cardioprotectionAndrew P Halestrap
Department of Biochemistry and The Bristol Heart Institute, University of Bristol, Bristol BS8 1TD, UK
Cardiovasc Res 61:372-85. 2004..However, only if subsequent MPTP closure occurs will ATP levels be maintained, ensuring that cell death continues down an apoptotic, rather than a necrotic, pathway...
- Transient mitochondrial permeability transition pore opening mediates preconditioning-induced protectionDerek Hausenloy
The Hatter Institute and Centre for Cardiology, University College London, UK
Circulation 109:1714-7. 2004..We hypothesize that transient mPTP opening and ROS mediate the protection associated with myocardial preconditioning and mitochondrial uncoupling...
- Role of glycogen synthase kinase-3beta in cardioprotectionMagdalena Juhaszova
Laboratory of Cardiovascular Science, Gerontology Research Center, Box 13, National Institute on Aging, NIH, Baltimore, Maryland 21224 6825, USA
Circ Res 104:1240-52. 2009....
- Structure at 2.8 A resolution of F1-ATPase from bovine heart mitochondriaJ P Abrahams
Medical Research Council Laboratory of Molecular Biology, Cambridge, UK
Nature 370:621-8. 1994..Interconversion of the states may be achieved by rotation of the alpha 3 beta 3 subassembly relative to an alpha-helical domain of the gamma-subunit...
- The mechanism of superoxide production by NADH:ubiquinone oxidoreductase (complex I) from bovine heart mitochondriaLothar Kussmaul
Medical Research Council Dunn Human Nutrition Unit, Wellcome Trust Medical Research Council Building, Hills Road, Cambridge CB2 2XY, United Kingdom
Proc Natl Acad Sci U S A 103:7607-12. 2006..we describe the kinetic and molecular mechanism of superoxide production by complex I isolated from bovine heart mitochondria and confirm that it produces predominantly superoxide, not hydrogen peroxide...
- The direct physiological effects of mitoK(ATP) opening on heart mitochondriaAlexandre D T Costa
Dept of Biology, Portland State Univ, PO Box 751, Portland, OR 97207, USA
Am J Physiol Heart Circ Physiol 290:H406-15. 2006..Here, we examine the evidence for these hypotheses through experiments on isolated rat heart mitochondria. Using perturbation techniques, we show that matrix volume is the consequence of a steady-state balance ..
- Energetic performance is improved by specific activation of K+ fluxes through K(Ca) channels in heart mitochondriaMiguel A Aon
The Johns Hopkins University, School of Medicine, Institute of Molecular Cardiobiology, 720 Rutland Ave, 1060 Ross Bldg, Baltimore, MD 21205 2195, USA
Biochim Biophys Acta 1797:71-80. 2010..by measuring K+ flux, membrane potential (DeltaPsi(m)), light scattering, and respiration in guinea pig heart mitochondria. K+ uptake and the influence of anions were assessed in mitochondria loaded with the K+ sensor PBFI by ..
- Exercise training induces respiratory substrate-specific decrease in Ca2+-induced permeability transition pore opening in heart mitochondriaMariannick Marcil
Départment de Kinesiology, Universite de Montreal, PO Box 6128 Centre Ville, Montreal, PQ, Canada H3C 3J7
Am J Physiol Heart Circ Physiol 290:H1549-57. 2006..to determine whether regular exercise (treadmill running, 10 wk) alters the susceptibility of rat isolated heart mitochondria to Ca(2+)-induced permeability transition pore (PTP) opening and whether this could be associated with ..
- Specific inhibition of the mitochondrial permeability transition prevents lethal reperfusion injuryLaurent Argaud
INSERM E 0226, Laboratoire de Physiologie Lyon Nord, Faculté de Médecine Lyon Nord, Universite Claude Bernard Lyon I, 8, avenue Rockefeller, 69373 Lyon Cedex 8, France
J Mol Cell Cardiol 38:367-74. 2005..These data indicate that specific inhibition of MPT pore opening at reperfusion following acute myocardial infarction provides a powerful antinecrotic and antiapoptotic protection...
- Mitochondrial PKCepsilon and MAPK form signaling modules in the murine heart: enhanced mitochondrial PKCepsilon-MAPK interactions and differential MAPK activation in PKCepsilon-induced cardioprotectionChristopher P Baines
Department of Physiology, University of Louisville, and the Jewish Hospital Heart and Lung Institute, Louisville, KY 40202, USA
Circ Res 90:390-7. 2002..Furthermore, formation of mitochondrial PKCepsilon-ERK modules appears to play a role in PKCepsilon-mediated cardioprotection, in part by the phosphorylation and inactivation of Bad...
- Analysis of the subunit composition of complex I from bovine heart mitochondriaJoe Carroll
Medical Research Council Dunn Human Nutrition Unit, The Wellcome Trust MRC Building, Hills Road, Cambridge CB2 2XY, United Kingdom
Mol Cell Proteomics 2:117-26. 2003Complex I purified from bovine heart mitochondria is a multisubunit membrane-bound assembly. In the past, seven of its subunits were shown to be products of the mitochondrial genome, and 35 nuclear encoded subunits were identified...
- 5-Hydroxydecanoate is metabolised in mitochondria and creates a rate-limiting bottleneck for beta-oxidation of fatty acidsPeter J Hanley
Institut fur Normale und Pathologische Physiologie, Universitat Marburg, Deutschhausstrasse 2, 35037 Marburg, Germany
J Physiol 562:307-18. 2005..using specially synthesised (and purified) substrates and enzymes, as well as isolated rat liver and heart mitochondria, and compared it with the metabolism of the physiological substrate decanoyl-CoA...
- Mitochondrial uncoupling, with low concentration FCCP, induces ROS-dependent cardioprotection independent of KATP channel activationJonathan P Brennan
Cardiac Physiology Cardiovascular Division, The Rayne Institute, St Thomas Hospital, King s College London, SE1 7EH, UK
Cardiovasc Res 72:313-21. 2006....
- Connexin 43 in cardiomyocyte mitochondria and its increase by ischemic preconditioningKerstin Boengler
Institut fur Pathophysiologie, Zentrum fur Innere Medizin, Universitatsklinikum Essen, Hufelandstr 55, 45122 Essen, Germany
Cardiovasc Res 67:234-44. 2005..Since mitochondria have been proposed to be involved in IP's protection, the present study analyzed whether Cx43 is localized at mitochondria of cardiomyocytes and whether such localization is affected by IP...
- Mitochondrial potassium transport: the role of the mitochondrial ATP-sensitive K(+) channel in cardiac function and cardioprotectionKeith D Garlid
Department of Biology, Portland State University, 1719 SW 10th Avenue, PO Box 751, Portland, OR 97207, USA
Biochim Biophys Acta 1606:1-21. 2003..MitoK(ATP)-mediated volume regulation, in turn, prevents disruption of the structure-function of the IMS and facilitates efficient energy transfers between mitochondria and myofibrillar ATPases...
- Anesthetic preconditioning improves adenosine triphosphate synthesis and reduces reactive oxygen species formation in mitochondria after ischemia by a redox dependent mechanismEnis Novalija
Medical College of Wisconsin, Department of Anesthesiology, M4280, 8701 Watertown Plank Road, Milwaukee, Wisconsin 53226, USA
Anesthesiology 98:1155-63. 2003....
- Heart mitochondria: gates of life and deathAsa B Gustafsson
BioScience Center San Diego State University 5500 Campanile Drive San Diego, CA 92182 4650, USA
Cardiovasc Res 77:334-43. 2008..In this review, we discuss the role of mitochondria in the control of cell death in cardiac myocytes...
- Mitochondrial DNA mutations, oxidative stress, and apoptosis in mammalian agingG C Kujoth
Departments of Genetics and Medical Genetics, University of Wisconsin, Madison, WI 53706, USA
Science 309:481-4. 2005..The levels of apoptotic markers were also found to increase during aging in normal mice. Thus, accumulation of mtDNA mutations that promote apoptosis may be a central mechanism driving mammalian aging...
- S-nitrosation of mitochondrial complex I depends on its structural conformationAlexander Galkin
Wolfson Institute for Biomedical Research, University College London, London, UK
J Biol Chem 282:37448-53. 2007..The implications of this finding for hypoxic or pathophysiological conditions in vivo are discussed...
- Modulation of the mitochondrial permeability transition pore complex in GSK-3beta-mediated myocardial protectionMasahiro Nishihara
Second Department of Internal Medicine, Sapporo Medical University School of Medicine, S 1 W 16, Chuo Ku, Sapporo 060 8543, Japan
J Mol Cell Cardiol 43:564-70. 2007..These results suggest that reduction in affinity of ANT to cyclophilin D by increased phospho-GSK-3beta binding to ANT may be responsible for suppression of mPTP opening and myocardial protection afforded by IPC+EPO...
- Akt mediated mitochondrial protection in the heart: metabolic and survival pathways to the rescueShigeki Miyamoto
Department of Pharmacology, University of California, 9500 Gilman Dr, La Jolla, San Diego, CA 92093 0636, USA
J Bioenerg Biomembr 41:169-80. 2009..In this review we discuss mechanisms by which Akt activation can effect changes at the mitochondria that protect cardiomyocytes and attenuate pathophysiological responses of the heart...
- Opening of the mitochondrial permeability transition pore causes depletion of mitochondrial and cytosolic NAD+ and is a causative event in the death of myocytes in postischemic reperfusion of the heartF Di Lisa
Consiglio Nazionale delle Ricerche Unit for the Study of Biomembranes, and the Department of Biological Chemistry, University of Padova, Italy
J Biol Chem 276:2571-5. 2001..The addition of Ca(2+) to isolated rat heart mitochondria resulted in a profound decrease in their NAD(+) content, which followed mitochondrial swelling...
- Cardioprotective signaling to mitochondriaKeith D Garlid
Department of Biology, Portland State University, Portland, OR 97201 0751, USA
J Mol Cell Cardiol 46:858-66. 2009..We review the experimental findings that bear on these hypotheses and other modes of protection involving mitochondria...
- The ratio of oxidative phosphorylation complexes I-V in bovine heart mitochondria and the composition of respiratory chain supercomplexesH Schagger
Zentrum der Biologischen Chemie, Universitatsklinikum Frankfurt, D 60590 Frankfurt, Germany
J Biol Chem 276:37861-7. 2001..c reductase (complex III), cytochrome c oxidase (complex IV), and F1F0-ATP synthase (complex V) from bovine heart mitochondria were determined by applying three novel and independent approaches that gave consistent results: 1) a ..
- Biochemical dysfunction in heart mitochondria exposed to ischaemia and reperfusionGiancarlo Solaini
Scuola Superiore di Studi Universitari e di Perfezionamento S Anna, Classe Accademica di Scienze Sperimentali, Piazza dei Martiri della Libertà 33, 56127 Pisa, Italy
Biochem J 390:377-94. 2005..Finally, we summarize the metabolic and pharmacological interventions that have been used to alleviate the effects of ischaemic injury, highlighting the value of these or related interventions in possible therapeutics...
- Peroxisome proliferator-activated receptor gamma coactivator-1 promotes cardiac mitochondrial biogenesisJ J Lehman
Department of Medicine, and Department of Pathology, Center for Cardiovascular Research, Washington University School of Medicine, St Louis, Missouri 63110, USA
J Clin Invest 106:847-56. 2000..These results identify PGC-1 as a critical regulatory molecule in the control of cardiac mitochondrial number and function in response to energy demands...
- Myocardial preconditioning against ischemia-reperfusion injury is abolished in Zucker obese rats with insulin resistancePrasad V G Katakam
Department of Physiology and Pharmacology, Wake Forest University Health Sciences, Hanes 1050, Medical Center Blvd, Winston Salem, NC 27157, USA
Am J Physiol Regul Integr Comp Physiol 292:R920-6. 2007..Thus obesity accompanied by IR is associated with the inability to precondition against ischemic cardiac injury, which is mediated by enhanced mitochondrial oxidative stress and impaired activation of mitochondrial K(ATP)...
- Decrease in mitochondrial complex I activity in ischemic/reperfused rat heart: involvement of reactive oxygen species and cardiolipinGiuseppe Paradies
Department of Biochemistry and Molecular Biology and CNR Institute of Biomembranes and Bioenergetics, University of Bari, Bari, Italy
Circ Res 94:53-9. 2004..These findings may provide an explanation for some of the factors responsible for myocardial reperfusion injury...
- Modulation of electron transport protects cardiac mitochondria and decreases myocardial injury during ischemia and reperfusionQun Chen
Cardiology Section, Medical Service 111 W, Louis Stokes VA Medical Center, 10701 East Blvd, Cleveland, OH 44106, USA
Am J Physiol Cell Physiol 292:C137-47. 2007..The initially counterintuitive approach to inhibit mitochondrial respiration provides a new cardioprotective paradigm to decrease cellular injury during both ischemia and reperfusion...
- Intramitochondrial signaling: interactions among mitoKATP, PKCepsilon, ROS, and MPTAlexandre D T Costa
Dept of Biology, Portland State Univ, PO Box 751, Portland, OR 97201 0751, USA
Am J Physiol Heart Circ Physiol 295:H874-82. 2008..This feedback pathway may be responsible for the lasting protective effect of preconditioning, colloquially known as the memory effect...
- Fo membrane domain of ATP synthase from bovine heart mitochondria: purification, subunit composition, and reconstitution with F1-ATPaseI R Collinson
MRC Laboratory of Molecular Biology, Cambridge, U K
Biochemistry 33:7971-8. 1994The Fo membrane domain of the F1Fo-ATP synthase complex has been purified from bovine heart mitochondria. The purification procedure involves the removal of peripheral membrane proteins, including F1-ATPase, from submitochondrial ..
- Molecular and cellular basis of the aetiology and management of diabetic cardiomyopathy: a short reviewErnest Adeghate
Department of Anatomy, Faculty of Medicine and Health Sciences, United Arab Emirates University, Al Ain, United Arab Emirates
Mol Cell Biochem 261:187-91. 2004....
- Ischemic defects in the electron transport chain increase the production of reactive oxygen species from isolated rat heart mitochondriaQun Chen
Department of Medicine, School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA
Am J Physiol Cell Physiol 294:C460-6. 2008..Thus ischemic damage to the ETC increased both the capacity and the net production of H(2)O(2) from complex I and complex III and sets the stage for an increase in ROS production during reperfusion as a mechanism of cardiac injury...
- Mitochondria: a target for myocardial protectionM S Suleiman
Bristol Heart Institute, University of Bristol, Bristol Royal Infirmary, Malborough Street, Bristol BS2 8HW, UK
Pharmacol Ther 89:29-46. 2001..Finally, we describe use of cardioplegic solutions in the clinical setting, and discuss how improved understanding of the aspects of mitochondrial function summarised above may lead to better protective strategies in the future...
- Electron transport chain defects in heart failureJordi Casademont
Muscle Research Unit, Department of Internal Medicine, Hospital Clinic, August Pi i Sunyer Biomedical Research Institute IDIBAPS, University of Barcelona, Catalonia, Spain
Heart Fail Rev 7:131-9. 2002..e. diastolic heart failure), as well as mitochondrial defects outside the electron transport chain (i.e., defects in Krebs cycle or beta-oxidation of fatty acids) are only approached circumstantially...
- Kynurenic acid influences the respiratory parameters of rat heart mitochondriaH Baran
Institute of Pharmacology and Toxicology, Veterinary University Vienna, Austria
Pharmacology 62:119-23. 2001..all investigated kynurenines, only kynurenic acid affected dose-dependently the respiratory parameters of heart mitochondria. Respiratory control and P/O values were reduced significantly with glutamate/malate and moderately with ..
- Bovine complex I is a complex of 45 different subunitsJoe Carroll
Dunn Human Nutrition Unit, The Medical Research Council, Hills Road, Cambridge CB2 2XY, United Kingdom
J Biol Chem 281:32724-7. 2006..Thus, the subunit composition of bovine complex I has been established. It is a complex of 45 different proteins plus non-covalently bound FMN and eight iron-sulfur clusters...
- Postconditioning inhibits mitochondrial permeability transitionLaurent Argaud
INSERM E 0226, Universite Claude Bernard Lyon I, France
Circulation 111:194-7. 2005..quot; After reflow, opening of the mitochondrial permeability transition pore (mPTP) has been involved in lethal reperfusion injury. We hypothesized that postconditioning may modulate mPTP opening...
- The post-translational modifications of the nuclear encoded subunits of complex I from bovine heart mitochondriaJoe Carroll
The Medical Research Council Dunn Human Nutrition Unit, Hills Road, Cambridge CB2 2XY, United Kingdom
Mol Cell Proteomics 4:693-9. 2005..These experiments represent another significant step toward establishing the precise chemical composition of mammalian complex I...
- Inhibiting mitochondrial permeability transition pore opening at reperfusion protects against ischaemia-reperfusion injuryDerek J Hausenloy
The Hatter Institute and Centre for Cardiology, University College London Hospitals and Medical School, Grafton Way, WC1E 6DB London, UK
Cardiovasc Res 60:617-25. 2003..We hypothesised that the novel immunosuppressant, sanglifehrin-A (SFA), given at the time of reperfusion, protects the myocardium from ischaemia-reperfusion injury, by suppressing mPTP opening...
- Complex I is the major site of mitochondrial superoxide production by paraquatHelena M Cocheme
Medical Research Council Dunn Human Nutrition Unit, Wellcome Trust MRC Building, Hills Road, Cambridge CB2 0XY, United Kingdom
J Biol Chem 283:1786-98. 2008..Together this membrane potential-dependent uptake across the mitochondrial inner membrane and the subsequent rapid reduction to the paraquat radical cation explain the toxicity of paraquat to mitochondria...
- Apoptosome formation and caspase activation: is it different in the heart?Lech Czerski
Department of Pathology and Comprehensive Cancer Center, The University of Michigan Medical School, Ann Arbor, MI 48109, USA
J Mol Cell Cardiol 37:643-52. 2004..Diminished expression of pro-apoptotic factors and/or expression of certain inhibitors of the apoptosome may raise the threshold for apoptosis in long-lived post-mitotic cells including myocytes of the heart...
- Changes in mitochondrial dynamics during ceramide-induced cardiomyocyte early apoptosisValentina Parra
Centro FONDAP Estudios Moleculares de la Celula, Universidad de Chile, Olivos 1007, Santiago 8380492, Chile
Cardiovasc Res 77:387-97. 2008..This process is associated with cell death. We investigated whether activation of apoptosis with ceramides affects mitochondrial dynamics and promotes mitochondrial fission in cardiomyocytes...
- Complex I within oxidatively stressed bovine heart mitochondria is glutathionylated on Cys-531 and Cys-704 of the 75-kDa subunit: potential role of CYS residues in decreasing oxidative damageThomas R Hurd
Medical Research Council Dunn Human Nutrition Unit, Wellcome Trust MRC Building, Hills Road, Cambridge CB2 0XY, United Kingdom
J Biol Chem 283:24801-15. 2008..Mass spectrometry of complex I from oxidatively stressed bovine heart mitochondria showed that only Cys-531 and Cys-704 were glutathionylated...
- The effects of ischaemic preconditioning, diazoxide and 5-hydroxydecanoate on rat heart mitochondrial volume and respirationKelvin H H Lim
The Bristol Heart Institute, Bristol Royal Infirmary, Malborough Street, Bristol BS2 8HW, UK
J Physiol 545:961-74. 2002..These data highlight the dangers of using 5HD and diazoxide as specific modulators of mitoK(ATP) channels in the heart...
- The pH hypothesis of postconditioning: staccato reperfusion reintroduces oxygen and perpetuates myocardial acidosisMichael V Cohen
Department of Physiology, MSB 3050, University of South Alabama, College of Medicine, Mobile, AL 36688, USA
Circulation 115:1895-903. 2007..Acidosis also suppresses MPTP formation. We tested whether postconditioning protects by maintaining acidosis during early reoxygenation...
- Myocardial ischemia selectively depletes cardiolipin in rabbit heart subsarcolemmal mitochondriaE J Lesnefsky
Division of Cardiology, Case Western Reserve University, Cleveland, Ohio 44106, USA
Am J Physiol Heart Circ Physiol 280:H2770-8. 2001..Cardiolipin content was preserved in IFM during ischemia. Thus cardiolipin is a relatively early target of ischemic mitochondrial damage, leading to loss of oxidative phosphorylation through cytochrome oxidase in SSM...
- Real-time 2-photon imaging of mitochondrial function in perfused rat hearts subjected to ischemia/reperfusionMadoka Matsumoto-Ida
Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine, 54 Kawahara cho, Shogoin, Sakyo ku, Kyoto 606 8507, Japan
Circulation 114:1497-503. 2006....
- Proteomic analysis of protein tyrosine nitration after ischemia reperfusion injury: mitochondria as the major targetBin Liu
Center for Biomedical EPR Spectroscopy and Imaging, Davis Heart and Lung Research Institute, and Division of Cardiovascular Medicine, Department of Internal Medicine, College of Medicine, The Ohio State University, Columbus, OH, 43210, USA
Biochim Biophys Acta 1794:476-85. 2009..Selective nitration of proteins from the oxidative phosphorylation system at the beginning of reperfusion may contribute to the suppression of oxygen consumption...
- Increased susceptibility to Ca(2+)-induced permeability transition and to cytochrome c release in rat heart mitochondria with aging: effect of melatoninGiuseppe Petrosillo
Department of Biochemistry and Molecular Biology, CNR Institute of Biomembranes and Bioenergetics, University of Bari, Italy
J Pineal Res 48:340-6. 2010..natural antioxidant, on the susceptibility to Ca(2+)-induced MPT opening and cytochrome c release in rat heart mitochondria. The mitochondrial content of normal and oxidized cardiolipin as a function of aging and melatonin treatment ..
- Compensated volume overload increases the vulnerability of heart mitochondria without affecting their functions in the absence of stressMariannick Marcil
Département de Kinésiologie, Universite de Montreal, C P 6128, Succursale Centre Ville, Montreal, Quebec, Canada H3C 3J7
J Mol Cell Cardiol 41:998-1009. 2006....
- Failure to precondition pathological human myocardiumS Ghosh
Department of Surgery, University Hospitals Leicester, United Kingdom
J Am Coll Cardiol 37:711-8. 2001....
- Aconitase and ATP synthase are targets of malondialdehyde modification and undergo an age-related decrease in activity in mouse heart mitochondriaConnie S Yarian
Department of Molecular Pharmacology and Toxicology, University of Southern California, 1985 Zonal Avenue, Los Angeles, CA 90033, USA
Biochem Biophys Res Commun 330:151-6. 2005..The biological consequences of an age-related decrease in aconitase and ATP synthase activities may contribute to the decline in mitochondrial bioenergetics evident during aging...
- Identification of a ryanodine receptor in rat heart mitochondriaG Beutner
Department of Pharmacology and Physiology, University of Rochester, School of Medicine and Dentistry, Rochester, New York 14642, USA
J Biol Chem 276:21482-8. 2001..In the presence of ryanodine, Ca(2+) uptake into isolated heart mitochondria is suppressed. In addition, ryanodine inhibited mitochondrial swelling induced by Ca(2+) overload...
- Role of the mitochondrial permeability transition in myocardial diseaseJames N Weiss
Cardiovascular Research Laboratory, Department of Medicine Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, Calif 90095 1760, USA
Circ Res 93:292-301. 2003..Investigations into this area are beginning to unravel some of the mechanistic links between cardioprotective signaling and mitochondria...
- Hyperglycemia-induced apoptosis in mouse myocardium: mitochondrial cytochrome C-mediated caspase-3 activation pathwayLu Cai
Department of Medicine, University of Louisville, Louisville, Kentucky, USA
Diabetes 51:1938-48. 2002..Hyperglycemia-induced myocardial apoptosis is mediated, at least in part, by activation of the cytochrome c-activated caspase-3 pathway, which may be triggered by ROS derived from high levels of glucose...
- The phosphorylation of subunits of complex I from bovine heart mitochondriaRuming Chen
Medical Research Council Dunn Human Nutrition Unit, Hills Road, Cambridge CB2 2XY, UK
J Biol Chem 279:26036-45. 2004In bovine heart mitochondria and in submitochondrial particles, membrane-associated proteins with apparent molecular masses of 18 and 10 kDa become strongly radiolabeled by [(32)P]ATP in a cAMP-dependent manner...
- Low rates of hydrogen peroxide production by isolated heart mitochondria associate with long maximum lifespan in vertebrate homeothermsAdrian J Lambert
Medical Research Council, Dunn Human Nutrition Unit, Hills Road, Cambridge CB2 2XY, UK
Aging Cell 6:607-18. 2007..We investigated this correlation by comparing rates of hydrogen peroxide (H(2)O(2)) production by heart mitochondria isolated from groups or pairs of species selected to have very different maximum lifespans but similar body ..
- Effect of the multitargeted tyrosine kinase inhibitors imatinib, dasatinib, sunitinib, and sorafenib on mitochondrial function in isolated rat heart mitochondria and H9c2 cellsYvonne Will
Exploratory Safety Differentiation, Pfizer, Inc, Groton, Connecticut 06340, USA
Toxicol Sci 106:153-61. 2008..Furthermore, we measured respiratory capacity of isolated rat heart mitochondria in the presence of the four kinase inhibitors and examined their effect on each of the oxidative ..
- The flavoprotein subcomplex of complex I (NADH:ubiquinone oxidoreductase) from bovine heart mitochondria: insights into the mechanisms of NADH oxidation and NAD+ reduction from protein film voltammetryChérise D Barker
Medical Research Council Dunn Human Nutrition Unit, Wellcome Trust MRC Building, Hills Road, Cambridge CB2 2XY, UK
Biochemistry 46:3454-64. 2007Complex I (NADH:ubiquinone oxidoreductase) from bovine heart mitochondria contains 45 different subunits and nine redox cofactors...
- Effects of desmin gene knockout on mice heart mitochondriaM Linden
Groupe de Biologie des Interactions Cellulaires, UMR CNRS 6558, Poitiers, France
J Bioenerg Biomembr 33:333-41. 2001..1997). In the present study we have isolated heart mitochondria from desmin null (D-/-) and control (D+/+) mice, and analyzed their composition by SDS-PAGE, immunoblotting, ..
- Inhibition of mitochondrial permeability transition prevents sepsis-induced myocardial dysfunction and mortalityJérôme Larché
EA 2689, Universite de Lille 2, Faculté de Médecine 1, Lille, France
J Am Coll Cardiol 48:377-85. 2006..Inhibition of mitochondrial permeability transition was achieved by means of pharmacological drugs and overexpression of the antiapoptotic protein B-cell leukemia (Bcl)-2...
- Reversible blockade of electron transport during ischemia protects mitochondria and decreases myocardial injury following reperfusionQun Chen
Department of Medicine, Division of Cardiology, School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA
J Pharmacol Exp Ther 319:1405-12. 2006..Reperfusion in the setting of preserved mitochondrial respiratory function attenuates the mitochondrial release of reactive oxygen species, enhances contractile recovery, and decreases myocardial infarct size...
- Sanglifehrin A acts as a potent inhibitor of the mitochondrial permeability transition and reperfusion injury of the heart by binding to cyclophilin-D at a different site from cyclosporin ASamantha J Clarke
Department of Biochemistry, School of Medical Sciences, University of Bristol, Bristol BS8 1TD, United Kingdom
J Biol Chem 277:34793-9. 2002..Because SfA does not inhibit calcineurin activity, our data suggest that it may be more desirable than CsA for protecting tissues recovering from ischemic episodes and for studying the role of the MPTP in cell death...
- Bax translocates to mitochondria of heart cells during simulated ischaemia: involvement of AMP-activated and p38 mitogen-activated protein kinasesMichela Capano
Department of Biochemistry and Molecular Biology, University College London, Gower Street, London WC1E 6BT, UK
Biochem J 395:57-64. 2006..It is concluded that Bax translocation to mitochondria is an early step in ischaemia and that it occurs in response to activation of p38 MAPK downstream of AMPK...
- Evidence for mitochondrial K+ channels and their role in cardioprotectionBRIAN O'ROURKE
Institute of Molecular Cardiobiology, Johns Hopkins University, 720 Rutland Ave, 844 Ross Bldg, Baltimore, MD 21205 2195, USA
Circ Res 94:420-32. 2004..This review updates recent progress in understanding the physiological role of mitoK(ATP) and highlights outstanding questions and controversies, with the intent of stimulating additional investigation on this topic...
- Overexpression of glutaredoxin-2 reduces myocardial cell death by preventing both apoptosis and necrosisNorbert Nagy
Cardiovascular Research Center, University of Connecticut, School of Medicine, Farmington, CT 06030 1110, USA
J Mol Cell Cardiol 44:252-60. 2008..The results indicated a crucial role of mitochondrial Glrx2 in cardioprotection...
- Diabetic cardiomyopathy revisitedSihem Boudina
Division of Endocrinology, Metabolism and Diabetes and Program in Human Molecular Biology and Genetics, University of Utah School of Medicine, Salt Lake City 84112, USA
Circulation 115:3213-23. 2007..This review discusses the latest findings in diabetic humans and in animal models and reviews emerging new mechanisms that may be involved in the development and progression of cardiac dysfunction in diabetes...
- Reactive oxygen species precede protein kinase C-delta activation independent of adenosine triphosphate-sensitive mitochondrial channel opening in sevoflurane-induced cardioprotectionR Arthur Bouwman
Department of Anesthesiology and the Laboratory for Physiology, Vrije Universiteit Medical Center Institute for Cardiovascular Research Vrije Universiteit, Amsterdam, The Netherlands
Anesthesiology 100:506-14. 2004....
- NHE-1 inhibition-induced cardioprotection against ischaemia/reperfusion is associated with attenuation of the mitochondrial permeability transitionSabzali Javadov
Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, University of Western Ontario, Medical Sciences Building, London, Ontario, Canada N6A 5C1
Cardiovasc Res 77:416-24. 2008..The possible contribution of the cardiac mitochondrial permeability transition pore (PTP) towards the cardioprotective effects of Na(+)-H(+) exchanger-1 (NHE-1) inhibition was studied in hearts subjected to ischaemia/reperfusion (IR)...
- Mitochondria as a target for the cardioprotective effects of nitric oxide in ischemia-reperfusion injuryLindsay S Burwell
Department of Biochemistry and Biophysics, University of Rochester Medical Center, Rochester, New York 14642, USA
Antioxid Redox Signal 10:579-99. 2008..These direct effects of NO* on mitochondria are the focus of this review...
- Zinc metallothionein imported into liver mitochondria modulates respirationB Ye
Center for Biochemical and Biophysical Sciences and Medicine, Harvard Medical School, Seeley G Mudd Building, 250 Longwood Avenue, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 98:2317-22. 2001..The presence and respiratory inhibition of MT in liver, but not heart, mitochondria suggest a hitherto unknown biological modulating activity of MT in cellular respiration and energy metabolism in a tissue-specific manner...
- Mitochondria and ischemia-reperfusion injury of the heart: fixing a holeFabio Di Lisa
Dipartimento di Chimica Biologica, Universita di Padova, Viale G Colombo 3, 35121 Padova
Cardiovasc Res 70:191-9. 2006..Here, we discuss our current understanding of the structure and function of PTP in the context of heart injury caused by ischemia and reperfusion...
- Mitochondrial energetics in the heart in obesity-related diabetes: direct evidence for increased uncoupled respiration and activation of uncoupling proteinsSihem Boudina
Division of Endocrinology, Metabolism, and Diabetes, Program in Human Molecular Biology and Genetics, University of Utah School of Medicine, Salt Lake City, Utah 84112, USA
Diabetes 56:2457-66. 2007..Mitochondrial uncoupling has been proposed to contribute to these metabolic abnormalities but has not been directly demonstrated...
- Investigation of the mechanism of proton translocation by NADH:ubiquinone oxidoreductase (complex I) from bovine heart mitochondria: does the enzyme operate by a Q-cycle mechanism?Steven Sherwood
Medical Research Council Dunn Human Nutrition Unit, Wellcome Trust MRC Building, Hills Road, Cambridge CB2 2XY, UK
Biochem J 400:541-50. 2006..Here, we describe experiments to determine whether complex I, isolated from bovine heart mitochondria, operates via a Q-cycle mechanism analogous to that observed in the cytochrome bc1 complex...
- Cardiac Fas-dependent and mitochondria-dependent apoptosis in ovariectomized ratsShin Da Lee
Department of Physical Therapy and Graduate Institute of Rehabilitation Science, China Medical University, Taichung, Taiwan
Maturitas 61:268-77. 2008..The purpose of this study was to evaluate whether cardiac Fas-dependent (type I) and mitochondria-dependent (type II) apoptotic pathways are activated in ovariectomized rats...
- Pharmacological and physiological stimuli do not promote Ca(2+)-sensitive K+ channel activity in isolated heart mitochondriaDouglas V Cancherini
Departamento de Bioquimica, Instituto de Quimica, Universidade de Sao Paulo, Sao Paulo, SP, Brazil
Cardiovasc Res 73:720-8. 2007..NS-1619 is cardioprotective, leading to the assumption that this effect is related to the opening of mitoK(Ca) channels. Here, we show several weaknesses in this hypothesis...
- Mitochondria are targets for geranylgeranylacetone-induced cardioprotection against ischemia-reperfusion in the rat heartTetsuji Shinohara
Department of Internal Medicine 1, Faculty of Medicine, Oita University, 1 1 Idaigaoka, Hasama, Oita 879 5593, Japan
Am J Physiol Heart Circ Physiol 293:H1892-9. 2007..These processes may involve opening of the mitoK(ATP) channel...
- Effects of NO on mitochondrial function in cardiomyocytes: Pathophysiological relevanceSean M Davidson
The Hatter Cardiovascular Institute, Department of Medicine, Royal Free and University College Medical School, 67 Chenies Mews, University College Hospital, London WC1E 6HX, United Kingdom
Cardiovasc Res 71:10-21. 2006....
- Role of apoptosis in cardiovascular diseaseYoungil Lee
BioScience Center, San Diego State University, San Diego, CA 92182 4650, USA
Apoptosis 14:536-48. 2009..This review provides a current overview of the evidence of apoptosis in cardiovascular diseases and discusses the molecular pathways involved in cardiac myocyte apoptosis...
- Release of cytochrome c from heart mitochondria is induced by high Ca2+ and peroxynitrite and is responsible for Ca(2+)-induced inhibition of substrate oxidationV Borutaite
Institute for Biomedical Research, Kaunas Medical University, Lithuania
Biochim Biophys Acta 1453:41-8. 1999..and other inducers of mitochondrial permeability transition cause the release of cytochrome c from isolated heart mitochondria. We found that 5 microM free Ca2+ induced changes in oxidative phosphorylation system similar to ischaemic ..
- Low complex I content explains the low hydrogen peroxide production rate of heart mitochondria from the long-lived pigeon, Columba liviaAdrian J Lambert
Medical Research Council Mitochondrial Biology Unit, Hills Road, Cambridge, CB2 0XY, UK
Aging Cell 9:78-91. 2010..this report, we investigate the underlying biochemical basis of the low hydrogen peroxide production rate of heart mitochondria from a long-lived species (pigeon) compared with a short-lived species with similar body mass (rat)...
- Cardiac mitochondrial damage and biogenesis in a chronic model of type 1 diabetesXia Shen
Dept of Pharmacology and Toxicology, University of Louisville, 570 S Preston St, Suite 304, Louisville, KY 40202, USA
Am J Physiol Endocrinol Metab 287:E896-905. 2004..Taken together, these results show that mitochondria are a primary target in the diabetic heart, probably due to oxidative stress, and that this damage coincides with and may stimulate mitochondrial biogenesis...
- Determination of the oxidation states of manganese in brain, liver, and heart mitochondriaThomas E Gunter
Department of Biochemistry and Biophysics, University of Rochester, School of Medicine and Dentistry, Rochester, New York 14642, USA
J Neurochem 88:266-80. 2004..While the presence of Mn3+ complexes cannot be proven in the spectrum of endogenous mitochondrial manganese, the shape of this spectrum could suggest the presence of Mn3+ near the limit of detection, probably as MnSOD...
- Disruption of a mitochondrial RNA-binding protein gene results in decreased cytochrome b expression and a marked reduction in ubiquinol-cytochrome c reductase activity in mouse heart mitochondriaFenghao Xu
Programme in Genetics and Genome Biology, Hospital for Sick Children, University of Toronto, Toronto, ON, Canada
Biochem J 416:15-26. 2008..This defines the site for PTCD2 action in mammalian mitochondria and suggests a possible role for dysfunction of this protein in the aetiology of heart failure...
- Photosensitization of intact heart mitochondria by the phthalocyanine Pc 4: Correlation of structural and functional deficits with cytochrome c releaseJunhwan Kim
Department of Biochemistry, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA
Free Radic Biol Med 49:726-32. 2010....
- Ischaemic preconditioning inhibits opening of mitochondrial permeability transition pores in the reperfused rat heartSabzali A Javadov
Department of Biochemistry, University of Bristol, Bristol BS8 1TD, UK
J Physiol 549:513-24. 2003..Our data suggest that protection from reperfusion injury is better achieved by reducing factors that induce MPTP opening than by inhibiting the MPTP directly...
- Acute temperature resistance threshold in heart mitochondria: Febrile temperature activates function but exceeding it collapses the membrane barrierRasa Zukiene
Centre of Environmental Research, Faculty of Natural Sciences, Vytautas Magnus University, LT 44404 Kaunas, Lithuania
Int J Hyperthermia 26:56-66. 2010..The aim of this study was to identify the components of mitochondrial oxidative phosphorylation affected by mild hyperthermia and to quantify the contribution of each component to changes in system behaviour...
- Effect of quercetin on daunorubicin-induced heart mitochondria changes in ratsJ Guzy
Department of Medical Chemistry and Biochemistry, Medical Faculty Safarik University, Kosice, Slovak Republic
Physiol Res 52:773-80. 2003..Quercetin also completely prevented daunorubicin-induced changes in fluorescence of the outer mitochondrial membrane. In conclusion, our data indicate that quercetin may be useful in mitigating daunorubicin-induced cardiotoxicity...
- Mitochondrial K(ATP) channels: role in cardioprotectionOlaf Oldenburg
Department of Physiology, MSB 3024, University of South Alabama, College of Medicine, Mobile 36688, USA
Cardiovasc Res 55:429-37. 2002..Thus the mK(ATP) probably serves a dual role as both a trigger and a mediator. Possible end-effectors of preconditioning's protection are discussed including the mK(ATP) itself...
- Relative contributions of heart mitochondria glutathione peroxidase and catalase to H(2)O(2) detoxification in in vivo conditionsFernando Antunes
Department of Molecular Pharmacology and Toxicology, School of Pharmacy, University of Southern California, Los Angeles, USA
Free Radic Biol Med 33:1260-7. 2002..Results show that the contribution of catalase to H(2)O(2) removal in heart mitochondria is not significant, even under strong oxidative conditions, such as those achieved in ischemia-reperfusion ..
- Heart mitochondria contain functional ATP-dependent K+ channelsZsombor Lacza
Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston Salem, NC 27157, USA
J Mol Cell Cardiol 35:1339-47. 2003..In the present study, we determined the presence of K(ATP)-channel subunits in mouse heart mitochondria, and investigated whether known openers or blockers of the channel can alter mitochondrial membrane ..
- The nitrated proteome in heart mitochondria of the db/db mouse model: characterization of nitrated tyrosine residues in SCOTYuan Wang
Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing, China
J Proteome Res 9:4254-63. 2010..2DE, Western blot, and mass spectrometry was implemented to survey the status of tyrosine nitration in mouse heart mitochondria. Compared to normal mice, nitrated proteins in the heart mitochondria of the db/db mouse model were ..
- Thiamine ameliorates diabetes-induced inhibition of pyruvate dehydrogenase (PDH) in rat heart mitochondria: investigating the discrepancy between PDH activity and PDH E1alpha phosphorylation in cardiac fibroblasts exposed to high glucoseYuka Kohda
Laboratory of Pharmacotherapy, Osaka University of Pharmaceutical Sciences, Takatsuki, Japan
J Pharmacol Sci 113:343-52. 2010..The O-glycosylation of PDH E1alpha may be involved in the regulation of the PDH activity...
- Blockade of electron transport before cardiac ischemia with the reversible inhibitor amobarbital protects rat heart mitochondriaQun Chen
Dept of Medicine, Cardiology Section, Medical Service 111 W, Case Western Reserve University, Louis Stokes Veterans Affairs Medical Center, 10701 East Boulevard, Cleveland, OH 44106, USA
J Pharmacol Exp Ther 316:200-7. 2006..5 mM. Amobarbital also preserved cytochrome c content in both SSM and IFM. Thus, reversible blockade of the electron transport chain during ischemia protects mitochondrial respiration...
- Bioenergetic remodeling of heart mitochondria by thyroid hormoneMichael J Goldenthal
The Molecular Cardiology and Neuromuscular Institute, Highland Park, NJ 08904, USA
Mol Cell Biochem 265:97-106. 2004..The marked, parallel increases in PPARalpha levels suggest its potential involvement in mediating myocardial-specific remodeling of mitochondria in response to T4...
- FCCP is cardioprotective at concentrations that cause mitochondrial oxidation without detectable depolarisationJonathan P Brennan
Cardiac Physiology Cardiovascular Division, King s College London, SE1 7EH, UK
Cardiovasc Res 72:322-30. 2006..Here we define the mitochondrial responses to increasing concentrations of FCCP and also to explore the equivalence of the cardioprotective doses of diazoxide...
- Endurance training limits the functional alterations of rat heart mitochondria submitted to in vitro anoxia-reoxygenationAntonio Ascensao
Department of Sport Biology, Faculty of Sport Sciences, University of Porto, Portugal
Int J Cardiol 109:169-78. 2006..The present study aimed to investigate the effect of moderate endurance treadmill training (14 weeks) against rat heart mitochondrial dysfunction induced by in vitro A-R...
- Arachidonic acid induces specific membrane permeability increase in heart mitochondriaMarco Di Paola
Institute of Biomembranes and Bioenergetics Consiglio Nazionale delle Ricerche Bari, Italy
FEBS Lett 580:775-81. 2006Micromolar concentrations of arachidonic acid cause in Ca2+ loaded heart mitochondria matrix swelling and Ca2+ release...
- NHE-1 inhibition improves impaired mitochondrial permeability transition and respiratory function during postinfarction remodelling in the ratSabzali Javadov
Department Physiology and Pharmacology, University of Western Ontario, London, Ont, Canada
J Mol Cell Cardiol 38:135-43. 2005..We conclude that NHE-1 inhibition has a protective effect on mitochondrial function, attenuating MPT pore opening and improving the respiratory function, which may contribute to the salutary effect of NHE-1 inhibitors in heart failure...
- The exogenous NADH dehydrogenase of heart mitochondria is the key enzyme responsible for selective cardiotoxicity of anthracyclinesH Nohl
Institute of Pharmacology and Toxicology, Veterinary University Vienna, Austria
Z Naturforsch C 53:279-85. 1998..The results presented in this study demonstrate that, in contrast to liver mitochondria, isolated heart mitochondria shuttle single electrons to adriamycin, giving rise to oxygen radical formation via autoxidation of ..
- The Jak/Stat Pathway and Mitochondrial FunctionANDREW CHARLES LARNER; Fiscal Year: 2013..Preliminary results with a transgenic mice that express Stat3 that is targeted heart mitochondria indicate that it the transgenic protein protects hearts from ischemia induced decreases in the activity of ..
- Metabolic Stress-Induced Fatty Acid Nitration and Cardiovascular FunctionMarsha P Cole; Fiscal Year: 2013..unreadable]NO-dependent oxidation and nitration products, nitrated fatty acids (NO2-FA), are generated in heart mitochondria under hyperglycemic conditions and can mediate reactions that beneficially modify mitochondrial function...
- Molecular Regulation of Cardiac KATP Channels in IschemiaJonathan C Makielski; Fiscal Year: 2012..a newly created panel of SUR2 antibodies and discovered novel short variants (Kd120, 68, 55, 28) in mouse heart mitochondria, with the SUR2-55 form uniquely in mitochondria and not the surface...
- Mechanisms underlie inverse gender discrepancy in ischemic protectionNian Qing Shi; Fiscal Year: 2010..splicing (IES) event in SUR2 mRNA to produce transcripts encoding the 55-kDa SUR2 short forms in heart mitochondria. Characterization of SUR2 KO has revealed an inverse pattern of gender difference in cardioprotection...
- BK(Ca) channel in heart mitochondriaLIGIA G TORO DE STEFANI; Fiscal Year: 2013..Further understanding of the underlying molecular mechanism(s) of mitoBKCa cardioprotective effects will provide new targets for translation into therapeutics. ..
- MITOCHONDRIAL IRON-SULFUR PROTEINSMichael Johnson; Fiscal Year: 1991..the functional, structural, electronic and magnetic properties of the multiple iron-sulfur centers in beef heart mitochondria. This will be accomplished by investigations of the membrane-bound enzymes of the mitochondrial electron ..
- Microxymetry Techniques for Cardiomocyte RespirationGovindasamy Ilangovan; Fiscal Year: 2005..production will also be studied using the proposed microxymetry; (ii) to study the respiration of isolated heart mitochondria using the proposed microxymtery...
- CALCIUM CONTROL IN MUSKRAT HEARTSTHOMAS MCKEAN; Fiscal Year: 1992..that mitochondria isolated from muskrat hearts have a greater calcium uptake capability than guinea pig heart mitochondria and this may be of benefit in the calcium overload which may occur during hypoxia, ischemia, acidosis and ..
- CONTROL MECHANISMS IN INTERMEDIARY METABOLISMEARL SHRAGO; Fiscal Year: 1990..Experiments will be carried out using liver and heart mitochondria, inverted submitochondrial particles and the purified ANT reconstituted into an artificial liposome system...
- ION TRANSPORT BY HEART MITOCHONDRIAGERALD BRIERLEY; Fiscal Year: 1993..proposal is to isolate and characterize three monovalent cation transporters of physiological importance in heart mitochondria. These are (a) the Na+/H+ antiport and (b) the Na+/Ca2+ antiport which, acting in concert contribute to ..
- Heart mitochondrial NOS and in vitro hypoxia/reperfusionPedram Ghafourifar; Fiscal Year: 2005..We will also test apoptosis, oxidative stress and peroxynitrite markers during hypoxia/reoxygenation in heart mitochondria of young and aged rats...
- BIOENERGETIC APPARATUS IN HEART MITOCHONDRIATSOO KING; Fiscal Year: 1990..It should be pointed out that this application (which differs from another project) emphasizes and deals with aspects of the non-cytochrome-containing components of the respiratory chain...
- Ultrafine Particles and Mitochondrial DysfunctionANNE JOHANSEN; Fiscal Year: 2005..Simultaneously, their toxicological effects will be tested in vitro on beef heart mitochondria, with particular interest on whether the initial mechanisms of mitochondrial dysfunction are lipid ..
- Antioxidant transgene in diabetic cardiomyopathyPaul Epstein; Fiscal Year: 2006..Agouti mice will be bred to mice protected by cardiac specific antioxidant transgenes to determine if oxidative damage is a requirement for cardiomyopathy in this model. ..
- FATTY ACID BETA-OXIDATION IN NORMAL & ISCHEMIC HEARTFRANKLIN HULL; Fiscal Year: 1980..fatty acid beta-oxidation by aerobic and ischemic isolated perfused rabbit hearts and by isolated rabbit heart mitochondria will be measured...
- CONTROL OF CARDIAC RESPIRATION BY CALCIUMRUSSELL SCADUTO; Fiscal Year: 1993..if the expected increase in mitochondrial Ca2+ would activate KGDH and stimulate M-A shuttle in isolated heart mitochondria. Finally, the applicant would study the relationship among cardiac O2 consumption, mitochondrial metabolism ..
- CROSS MODULATION OF EXCITABILITY AND CA IN HEART FAILUREBRIAN O ROURKE; Fiscal Year: 2007..Elucidation of the molecular details of the regulation of cardiac excitation-contraction coupling will help us to fulfill our long term goal of restoring normal contractile function to the failing heart. ..
- ENERGETIC REGULATION OF CARDIAC ION CHANNELSBRIAN O ROURKE; Fiscal Year: 2004..Understanding this important, but heretofore understudied, problem will ultimately lend insight into all aspects of cardiac pathophysiology. ..
- FUNCTION AND REGULATION OF UNCOUPLING PROTEINS 2 AND 3Keith Garlid; Fiscal Year: 2006..These studies will provide new understanding of the mechanisms of UCP2 and 3 function and regulation and will also resolve mechanistic questions that have been raised about these proteins. ..
- The Mitochondrial ATP-Sensitive K+ Channel in HeartKeith D Garlid; Fiscal Year: 2010..Identification of signaling intermediates will utilize 32P-labeling and functional assays of phosphorylation. ..
- CARDIOMYOPATHY IN AIDSWilliam Lewis; Fiscal Year: 2009..HYPOTHESIS 4: mtDNA depletion (from any above) causes or results from oxidative stress. Antioxidants ameliorate oxidative stress from NRTIs by decreasing oxidation of mtDNA. ..
- Mitochondrial Role in Manganese ToxicityThomas Gunter; Fiscal Year: 2010....
- Acquired mtDNA depletion and nucleoside reverse transciptase inhibitorsWilliam Lewis; Fiscal Year: 2010..Experiments offer insights into improving therapy with antiretrovirals used in AIDS. ..
- STRUCTURE/FUNCTION OF THE MITOCHONDRIAL K-ATP CHANNELKeith Garlid; Fiscal Year: 2001..K+ flux will also be measured in intact mitochondria in order to examine the physiological role of mitoKATP using control analysis. ..
- Nucleoside analogs, mitochondria and AIDS cardiomyopathyWilliam Lewis; Fiscal Year: 2006..AIM 2: to define CM from HAART microscopically and ultrastructurally using morphometric methods. AIM 3: to define cardiac performance in CM from HAART echocardiographically and using Langendorff preparations. ..
- CARDIAC DYSFUNCTION, AIDS AND COCAINEWilliam Lewis; Fiscal Year: 2003..Immuno-LM and immuno-TEM identify cellular and subcellular alterations. ..
- Hepatic mitochondrial oxidative stress, AIDS and alcoholWilliam Lewis; Fiscal Year: 2005..Biochemical, molecular and pathological changes (above) are ameliorated. This serves as a "proof of principle". ..
- AIDS and Alcohol and CardiomyopathyWilliam Lewis; Fiscal Year: 2005..Myofibrillar, nuclear and mitochondrial volumes are analyzed quantitatively (by transmission electron microscopy [TEM]). Volume fractions of extracellular matrix and of myocytes are determined morphometrically (light and TEM). ..
- Effect of Drugs on Myocardial HypoxiaGarrett Gross; Fiscal Year: 2009..Information gained from these studies will hopefully lead to new therapies to treat patients with ischemic heart disease. ..
- PHOSPHOLIPASE C AND CARDIAC HYPERTROPHYGERALD DORN; Fiscal Year: 2005..abstract_text> ..
- NRTI-induced Mitochondrial CardiomyopathyKendall Wallace; Fiscal Year: 2006..abstract_text> ..
- Abnormalities of Mitochondria in Chagasic MyocarditisNisha Garg; Fiscal Year: 2003..The proposed studies will determine the pathophysiological contribution of host mitochondrial abnormalities in the progression of chagas disease. ..
- PROTON & ELECTRON TRANSFER & ENERGY COUPLING IN SITE ITOMOKO NONE OHNISHI; Fiscal Year: 2010..Complex I is the major site of superoxide generation in brain and heart mitochondria, but no consensus has been attained regarding the generation site(s)...
- ADRIAMYCIN-INDUCED MITOCHONDRIAL CARDIOMYOPATHYKendall Wallace; Fiscal Year: 2004....
- Calpains as Mediators of Cardiac Ischemic InjuryGerald W Dorn; Fiscal Year: 2010..Collectively, these studies will apply state-of-the-art techniques for in vivo genetic manipulation, microphysiologic analysis, and biochemical assessment to achieve insight into the roles of myocardial calpains in health and disease. ..
- Protein Radical, Protein Nitration, Mitochondria, and ADYeong Renn Chen; Fiscal Year: 2004..The results will provide fundamental information concerning the pathological relevance of neurodegenerative disease, such as AD, associated with mitochondrial dysfunction caused by oxidative damage. ..
- Metabolism of Hypertrophic Hearts Overexpressing SERCAJ O DONNELL; Fiscal Year: 2009..Our long term goal is: to identify the specific mechanisms of metabolic uncoupling in hypertrophic heart as potential targets for therapeutic intervention. ..
- CATECHOLS AND ADENOSINE IN MYOCARDIAL PRECONDITIONINGMichael Cohen; Fiscal Year: 2006..Finally, I will see if NECA's salvage of myocardium at reperfusion translates into rapid functional benefits. It is hoped that the potential of this new pharmacologic approach can be defined. ..
- Study of Intrinsic Bladder Activity by Optical ImagingAnthony Kanai; Fiscal Year: 2007..To study the neural-chemical control of spontaneous detrusor activity; and III.) To determine the origin of detrusor overactivity in partially obstructed bladders. ..
- Cancer-Related Glycolytic Gene:Regulation and TargetingPeter Pedersen; Fiscal Year: 2008..abstract_text> ..
- Internat'l symposium:vascular neuroeffector mechanismsSUE DUCKLES; Fiscal Year: 2002..We anticipate that all aspects of this conference will help to foster development of new directions and collaborations in the field. ..
- REGULATION OF AEROBIC GENE EXPRESSION BY MUSCLE ACTIVITYJohn Kennedy; Fiscal Year: 2002..Expression of transcription factors (novel or known) will be examined by Northern blotting of mRNA levels and evaluation of the response of aerobic gene promoters to forced expression of these regulatory factors. ..
- Exercise, Antioxidants, and I-R InjuryScott Powers; Fiscal Year: 2006..abstract_text> ..
- Imaging Apoptosis to Detect Unstable Atheromatous PlaqueJagat Narula; Fiscal Year: 2004..The impending surgical intervention will allow histopathological evaluation of the endarterectomy specimens to define potential utility of annexin imaging. ..
- Mitochondria and Cardiac Cell DeathJames Weiss; Fiscal Year: 2007..unreadable] [unreadable]..
- Factor B and energy coupling in mitochondriaGRIGORY BELOGRUDOV; Fiscal Year: 2007..The proposed research is expected to advance the knowledge of the molecular mechanisms of energy transfer and conservation in mitochondria, and shed light on the role of mitochondria in a number of human disorders. ..
- MOLEC GENETICS OF COMPLEX I IN MAMMALIAN MITOCHONDRIAImmo Scheffler; Fiscal Year: 2004..Such mice promise to become model systems for mitochondrial diseases. 5) Known cDNAs will be tested to identify the defective gene in the other four complementation groups with complex I defects. ..
- MAPK/PKR Modulation of Diaphragm WeaknessGerald S Supinski; Fiscal Year: 2010..We will both characterize the effects of inflammation on DISC formation, localization, and autocatalytic activity and determine if these alterations can be blocked by inhibition of p38, JNK, and/or PKR signaling pathways. ..
- Mitochondrial Protection Within Chronically Ischemic MyocardiumEdward O McFalls; Fiscal Year: 2010..Using this model, we propose that a class of drugs used in diabetic patients that has been associated with heart failure exacerbations, alters the mitochondrial energy production in a similar way. ..
- PROPERTIES OF INWARD RECTIFIER K CHANNELSJames Weiss; Fiscal Year: 2007..abstract_text> ..
- Role of Caspase-9 in HeartPeter Kang; Fiscal Year: 2005..Thus, the cardiac specific knockout of caspase-9 using Cre-loxP technology allows us to examine the tissue-specific role of capase-9 in adult animal. ..
- MSM Multiscale Modeling of the Heart in CardiovascularDANIEL BEARD; Fiscal Year: 2007..abstract_text> ..
- THE ROLE OF SULFATIDES IN ALZHEIMER'S DISEASEXianlin Han; Fiscal Year: 2008..abstract_text> ..
- Postsynthetic Modifications of Bacterial Membrane LipidsJohn Cronan; Fiscal Year: 2006..These processes will be studied by a combination of biochemical, genetic, and molecular biological approaches including tests of pathogenesis in a mouse model system ..
- Mechanical Ventilation and Diaphragmatic Oxidant InjuryScott Powers; Fiscal Year: 2008..abstract_text> ..
- Regulation of Liver CPT-I during Diabetic KetosisCharles Hoppel; Fiscal Year: 2008..The proposed studies will establish at the molecular and biochemical level the phosphorylation cycle of CPT-I and how it relates to the kinetics of CPT-I in liver. ..
- Mg2+ homeostasis in liver cells treated with EtOHAndrea Romani; Fiscal Year: 2009....