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Genomes and Genes | Elizabeth MurphySummaryAffiliation: National Institutes of Health Country: USA Publications
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Publications
S-nitrosylation: a radical way to protect the heartElizabeth Murphy
Cardiac Physiology Section, Systems Biology Center, NHLBI, NIH, Bethesda, MD 20892, USA
J Mol Cell Cardiol 52:568-77. 2012..The role of nitric oxide synthase uncoupling in cardioprotection will also be addressed. This article is part of a Special Section entitled "Post-translational Modification."..- What makes the mitochondria a killer? Can we condition them to be less destructive?Elizabeth Murphy
Translational Medicine Branch, NHLBI, NIH, Bethesda, MD 20892, USA
Biochim Biophys Acta 1813:1302-8. 2011..This article is part of a Special Issue entitled: Mitochondria and Cardioprotection... - Sex differences in the phosphorylation of mitochondrial proteins result in reduced production of reactive oxygen species and cardioprotection in femalesClaudia J Lagranha
Translational Medicine Branch, NHLBI NIH 10 Center Bethesda, MD 20892, USA
Circ Res 106:1681-91. 2010..Although premenopausal females have a lower risk for cardiovascular disease, the mechanism(s) are poorly understood... - Disruption of caveolae blocks ischemic preconditioning-mediated S-nitrosylation of mitochondrial proteinsJunhui Sun
Systems Biology Center, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
Antioxid Redox Signal 16:45-56. 2012..Mitochondria are key regulators of preconditioning, and most proteins showing an increase in SNO with IPC are mitochondrial. The aim of this study was to address how IPC transduces NO/SNO signaling to mitochondria in the heart... - Measurement of S-nitrosylation occupancy in the myocardium with cysteine-reactive tandem mass tags: short communicationMark J Kohr
Laboratory of Cardiac Physiology, Systems Biology Center, National Heart Lung and Blood Institute, Bethesda, MD 20892, USA
Circ Res 111:1308-12. 2012..However, little is known with regard to the percentage of a given protein that is modified by SNO (ie, SNO occupancy). Current methods allow for the relative quantification of SNO levels, but not for the determination of SNO occupancy... 
Preconditioning results in S-nitrosylation of proteins involved in regulation of mitochondrial energetics and calcium transportJunhui Sun
NHLBI, NIH, Vascular Medicine Branch, Bethesda, MD 20892, USA
Circ Res 101:1155-63. 2007..IPC and GSNO produced a similar pattern of S-nitrosylation modification and cardiac protection against ischemia/reperfusion injury, suggesting that protein S-nitrosylation may play an important cardioprotective role in heart...- Acute inhibition of GSK causes mitochondrial remodelingTiffany Nguyen
Systems Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA
Am J Physiol Heart Circ Physiol 302:H2439-45. 2012..Taken together, these data show that SB leads to a remodeling of the mitochondrial proteome that is partially GD sensitive... - Mechanism of cardioprotection: what can we learn from females?Elizabeth Murphy
NHLBI, NIH, Room 8N202, Building 10, 10 Center Drive, Bethesda, MD, USA
Pediatr Cardiol 32:354-9. 2011..It investigates estrogen signaling mediated by the nuclear estrogen receptors alpha and beta and the G-protein-coupled receptor (GPR 30/GPER). Estrogen signaling via nitric oxide and the PI3K pathway are discussed... - Cardioprotection leads to novel changes in the mitochondrial proteomeRenee Wong
Translational Medicine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
Am J Physiol Heart Circ Physiol 298:H75-91. 2010..Thus the ability of PC and GSK inhibition to alter the expression levels of electron transport complexes will have important implications for mitochondrial function... - Activation of a novel estrogen receptor, GPER, is cardioprotective in male and female ratsAnne M Deschamps
National Institutes of Health, National Heart, Lung, and Blood Institute, Translational Medicine Branch, Laboratory of Cardiac Physiology, Bethesda, MD 20892, USA
Am J Physiol Heart Circ Physiol 297:H1806-13. 2009..Taken together, the data show that G-1 activation of GPER improves functional recovery and reduces infarct size in isolated rat hearts following I/R through a PI3K-dependent, gender-independent mechanism... - Cysteine 203 of cyclophilin D is critical for cyclophilin D activation of the mitochondrial permeability transition poreTiffany T Nguyen
Systems Biology Center, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 286:40184-92. 2011..Our results indicate that the Cys-203 residue of CypD is necessary for redox stress-induced activation of mPTP... - Calcium-sensing receptor: a sensor and mediator of ischemic preconditioning in the heartJunhui Sun
Translational Medicine Branch, National Heart Lung and Blood Institute, National Institutes of Health, Bldg 10 Rm 8N206, Bethesda, MD 20892, USA
Am J Physiol Heart Circ Physiol 299:H1309-17. 2010..Taken together, the distribution of CaSR in caveolae along with NPS2143-blockade of IPC-induced cardioprotective signaling suggest that the activation of CaSR during IPC is cardioprotective by a process involving caveolae... - Estrogen receptor activation and cardioprotection in ischemia reperfusion injuryAnne M Deschamps
National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
Trends Cardiovasc Med 20:73-8. 2010..In this review, we will focus on the signaling pathways leading to cardioprotection in ischemia reperfusion injury after ER activation and discuss the possibility and promise of specific ER modulators to treat ischemic heart diseases... - Protein S-nitrosylation and cardioprotectionJunhui Sun
Translational Medicine Branch, NHLBI, NIH, 10 Center Dr, Room 7N112, Bethesda, MD 20892, USA
Circ Res 106:285-96. 2010..A better understanding of the mechanism regulating protein S-nitrosylation and its role in cardioprotection will provide us new therapeutic opportunities and targets for interventions in cardiovascular diseases... - Mechanisms underlying acute protection from cardiac ischemia-reperfusion injuryElizabeth Murphy
Vascular Medicine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, USA
Physiol Rev 88:581-609. 2008..Preconditioning activates a number of signaling pathways that reduce Ca(2+) overload and reduce activation of the mitochondrial permeability transition pore. The mitochondrial targets of cardioprotective signals are discussed in detail... - Myristoylated methionine sulfoxide reductase A protects the heart from ischemia-reperfusion injuryHang Zhao
Laboratory of Biochemistry, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892 8012, USA
Am J Physiol Heart Circ Physiol 301:H1513-8. 2011..We conclude that cytosolic MsrA protects the heart from ischemia-reperfusion damage. The requirement for myristoylation suggests that MsrA must interact with a hydrophobic domain to provide protection... - Cardioprotection in females: a role for nitric oxide and altered gene expressionElizabeth Murphy
Head Cardiac Physiology Section, Vascular Medicine Branch, National Heart, Lung, and Blood Institute NIH, 10 Center Drive, Bethesda, MD 20892, USA
Heart Fail Rev 12:293-300. 2007..Taken together, estrogen by genomic and non-genomic pathways can result in the initiation of a number of signaling pathways that enhance cardioprotection... - What can we learn about cardioprotection from the cardiac mitochondrial proteome?Marjan Gucek
NHLBI Proteomics Core, NHLBI, NIH, 10 Center Drive, Bethesda, MD 20892, USA
Cardiovasc Res 88:211-8. 2010..We focus on the cardiac mitochondrial proteome with emphasis on changes associated with cell death and protection, and we summarize how proteomic data have contributed to addressing the role of mitochondria in cardioprotection... - CypD(-/-) hearts have altered levels of proteins involved in Krebs cycle, branch chain amino acid degradation and pyruvate metabolismSara Menazza
Systems Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA
J Mol Cell Cardiol 56:81-90. 2013..In summary, CypD(-/-) hearts exhibit changes in many metabolic pathways and caution should be used when interpreting results from these mice as due solely to inhibition of the MPTP... - Essential role of nitric oxide in acute ischemic preconditioning: S-nitros(yl)ation versus sGC/cGMP/PKG signaling?Junhui Sun
Systems Biology Center, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
Free Radic Biol Med 54:105-12. 2013..In conclusion, these results suggest that the protective effect of NO is not related primarily to activation of the sGC/cGMP/PKG signaling pathway, but rather through SNO signaling in IPC-induced acute cardioprotection... - Mitochondrial permeability transition pore and calcium handlingRenee Wong
Cardiac Physiology Section, Systems Biology Center, NHLBI, NIH, Bethesda, MD 20892, USA
Methods Mol Biol 810:235-42. 2012..This chapter focuses on key issues in the study of the MPT and provides some methods for measuring MPT opening in isolated mitochondria... - Does inhibition of glycogen synthase kinase protect in mice?Elizabeth Murphy
Vascular Medicine Branch, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD 20892, USA
Circ Res 103:226-8. 2008 - The role of comorbidities in cardioprotectionMichael N Sack
Center for Molecular Medicine, NHLBI, NIH, Bethesda, MD, USA
J Cardiovasc Pharmacol Ther 16:267-72. 2011..It is important to understand at a mechanistic level the reasons for these differences. The effects of sex and diseases need to be considered in design of cardioprotective interventions in animal studies and clinical trials... - Is Na/Ca exchange during ischemia and reperfusion beneficial or detrimental?Elizabeth Murphy
Laboratory of Signal Transduction, National Institute for Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA
Ann N Y Acad Sci 976:421-30. 2002..These studies suggest that overexpression of the Na/Ca exchanger enhances injury in males, but females are protected by a gender-related mechanism... - Primary and secondary signaling pathways in early preconditioning that converge on the mitochondria to produce cardioprotectionElizabeth Murphy
Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, US Department of Health and Human Services, Research Triangle Park, NC, USA
Circ Res 94:7-16. 2004..Alterations in these mitochondrial proteins results in altered metabolism and inhibition of cell death, thus resulting in cardioprotection... - Inhibit GSK-3beta or there's heartbreak dead aheadElizabeth Murphy
Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina 27709, USA
J Clin Invest 113:1526-8. 2004..The phosphorylation and inhibition of GSK-3beta lead to inhibition or delayed activation of the mitochondrial permeability transition, a key regulator of apoptosis... - Acute hemorrhagic myocardial necrosis and sudden death of rats exposed to a combination of ephedrine and caffeineAbraham Nyska
Laboratory of Experimental Pathology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
Toxicol Sci 83:388-96. 2005..Our work shows the direct relationship between combined ephedrine and caffeine exposure and cardiac pathology... - Bcl-2 regulation of mitochondrial energeticsElizabeth Murphy
Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA
Trends Cardiovasc Med 15:283-90. 2005..Understanding the physiologic processes controlled by Bcl-2 will be important in understanding cell regulation, and it may also provide new insights into the regulation of apoptosis... - S-nitrosylation: NO-related redox signaling to protect against oxidative stressJunhui Sun
National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
Antioxid Redox Signal 8:1693-705. 2006..However, oxidative stress and the resultant dysfunction of NO signaling have been implicated in the pathogenesis of cardiovascular diseases... - Preconditioning: the mitochondrial connectionElizabeth Murphy
National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA
Annu Rev Physiol 69:51-67. 2007..This review focuses on mechanisms by which cardioprotection alters mitochondrial proteins and channels that regulate cell death and survival... - Does the voltage dependent anion channel modulate cardiac ischemia-reperfusion injury?Samarjit Das
Department of Pathology, Johns Hopkins Medical Institute and Systems Biology Center, NHLBI, NIH, Bethesda, MD, USA
Biochim Biophys Acta 1818:1451-6. 2012..This article is part of a Special Issue entitled: VDAC structure, function, and regulation of mitochondrial metabolism... - Treatment with an estrogen receptor-beta-selective agonist is cardioprotectiveIvana Nikolic
Laboratory of Signal Transduction, NIEHS, NIH, DHHS, Durham, NC, USA
J Mol Cell Cardiol 42:769-80. 2007..Gene profiling showed that treatment with DPN resulted in upregulation of a number of protective genes such as heat shock protein 70, the antiapoptotic protein, growth arrest and DNA damage 45 beta, and cyclooxygenase 2... - Estrogen signaling and cardiovascular diseaseElizabeth Murphy
Cardiac Physiology Section, Systems Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
Circ Res 109:687-96. 2011..This article reviews the different estrogen receptors and their signaling mechanisms, discusses mechanisms that regulate estrogen receptor levels and locations, and considers the cardiovascular effects of estrogen signaling... - Ion transport and energetics during cell death and protectionElizabeth Murphy
National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, USA
Physiology (Bethesda) 23:115-23. 2008..This review will discuss mechanisms involved in alterations in ions and high energy phosphate metabolites in perfused or intact heart during ischemia and reperfusion... - Gender-based differences in mechanisms of protection in myocardial ischemia-reperfusion injuryElizabeth Murphy
Vascular Medicine Branch, NHLBI, NIH, DHHS, Bethesda, MD 20892, USA
Cardiovasc Res 75:478-86. 2007..This review will summarize the data showing protection in females in animal studies and will summarize the data on possible mechanisms of cardioprotection in females... - Deoxymyoglobin is a nitrite reductase that generates nitric oxide and regulates mitochondrial respirationSruti Shiva
Vascular Medicine Branch, Clinical Center National Institutes of Health, Bethesda, MD 20892 1662, USA
Circ Res 100:654-61. 2007.... - Inhibition of GSK-3beta as a target for cardioprotection: the importance of timing, location, duration and degree of inhibitionElizabeth Murphy
National Institute of Environmental Health Sciences, Laboratory of Signal Transduction, NIH, DHHS, Research Triangle Park, NC 27709, USA
Expert Opin Ther Targets 9:447-56. 2005..Therapies for inhibiting GSK are feasible as there are a number of newly developed specific inhibitors of GSK available, although most of these drugs have not been tested in long-term animal studies... - Transient upregulation of PGC-1alpha diminishes cardiac ischemia tolerance via upregulation of ANT1Edward G Lynn
Translational Medicine Branch, NHLBI, NIH, Bethesda, MD 20892 1454, USA
J Mol Cell Cardiol 49:693-8. 2010..These adverse phenotypes appear to be mediated, in part, by PGC-1alpha induced upregulation of ANT1... - Regulation of intracellular and mitochondrial sodium in health and diseaseElizabeth Murphy
Translational Medicine Branch, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD 20892, USA
Circ Res 104:292-303. 2009..Although much has been learned about sodium regulation in the heart, there are still many unanswered questions, particularly concerning mitochondrial Na regulation...