J J Lemasters

Summary

Affiliation: University of North Carolina
Country: USA

Publications

  1. ncbi The mitochondrial permeability transition in cell death: a common mechanism in necrosis, apoptosis and autophagy
    J J Lemasters
    Department of Cell Biology and Anatomy, University of North Carolina at Chapel Hill, CB No 7090, 236 Taylor Hall, Chapel Hill, NC 27799 7090, USA
    Biochim Biophys Acta 1366:177-96. 1998
  2. ncbi Mitochondrial dysfunction in the pathogenesis of necrotic and apoptotic cell death
    J J Lemasters
    Department of Cell Biology and Anatomy, University of North Carolina at Chapel Hill, 27799 7090, USA
    J Bioenerg Biomembr 31:305-19. 1999
  3. ncbi Selective mitochondrial autophagy, or mitophagy, as a targeted defense against oxidative stress, mitochondrial dysfunction, and aging
    John J Lemasters
    Department of Cell and Developmental Biology, School of Medicine, University of North Carolina, Chapel Hill, North Carolina 27599 7090, USA
    Rejuvenation Res 8:3-5. 2005
  4. ncbi Role of mitochondrial inner membrane permeabilization in necrotic cell death, apoptosis, and autophagy
    John J Lemasters
    Department of Cell and Developmental Biology, University of North Carolina, Chapel Hill, North Carolina 27599 7090, USA
    Antioxid Redox Signal 4:769-81. 2002
  5. ncbi Dying a thousand deaths: redundant pathways from different organelles to apoptosis and necrosis
    John J Lemasters
    Department of Cell and Developmental Biology, University of North Carolina at Chapel Hill, 27599 7090, USA
    Gastroenterology 129:351-60. 2005
  6. ncbi Prevention of hepatic ischemia-reperfusion injury by green tea extract
    Zhi Zhong
    Department of Cell and Developmental Biology, University of North Carolina at Chapel Hill, 27599, USA
    Am J Physiol Gastrointest Liver Physiol 283:G957-64. 2002
  7. ncbi Screening assays for the mitochondrial permeability transition using a fluorescence multiwell plate reader
    J R Blattner
    Department of Cell Biology and Anatomy, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7090, USA
    Anal Biochem 295:220-6. 2001
  8. ncbi Role of the mitochondrial permeability transition in apoptotic and necrotic death after ischemia/reperfusion injury to hepatocytes
    J S Kim
    Department of Cell and Developmental Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 7090, USA
    Curr Mol Med 3:527-35. 2003
  9. ncbi Primary cirrhotic hepatocytes resist TGFbeta-induced apoptosis through a ROS-dependent mechanism
    Dalliah Black
    Division of Gastrointestinal Surgery, Department of Surgery, University of North Carolina, 320 Medical Wing E, Chapel Hill, NC 27599 7081, USA
    J Hepatol 40:942-51. 2004
  10. ncbi The mitochondrial permeability transition initiates autophagy in rat hepatocytes
    S P Elmore
    Department of Cell and Developmental Biology and Curriculum in Toxicology, University of North Carolina, Chapel Hill, NC 27599, USA
    FASEB J 15:2286-7. 2001

Collaborators

Detail Information

Publications80

  1. ncbi The mitochondrial permeability transition in cell death: a common mechanism in necrosis, apoptosis and autophagy
    J J Lemasters
    Department of Cell Biology and Anatomy, University of North Carolina at Chapel Hill, CB No 7090, 236 Taylor Hall, Chapel Hill, NC 27799 7090, USA
    Biochim Biophys Acta 1366:177-96. 1998
    ..A model is proposed in which onset of the MPT to increasing numbers of mitochondria within a cell leads progressively to autophagy, apoptosis and necrotic cell death...
  2. ncbi Mitochondrial dysfunction in the pathogenesis of necrotic and apoptotic cell death
    J J Lemasters
    Department of Cell Biology and Anatomy, University of North Carolina at Chapel Hill, 27799 7090, USA
    J Bioenerg Biomembr 31:305-19. 1999
    ....
  3. ncbi Selective mitochondrial autophagy, or mitophagy, as a targeted defense against oxidative stress, mitochondrial dysfunction, and aging
    John J Lemasters
    Department of Cell and Developmental Biology, School of Medicine, University of North Carolina, Chapel Hill, North Carolina 27599 7090, USA
    Rejuvenation Res 8:3-5. 2005
    ..For this selective autophagy of mitochondria, we propose the term "mitophagy" to emphasize the non-random nature of the process. Mitophagy may play a key role in retarding accumulation of somatic mutations of mtDNA with aging...
  4. ncbi Role of mitochondrial inner membrane permeabilization in necrotic cell death, apoptosis, and autophagy
    John J Lemasters
    Department of Cell and Developmental Biology, University of North Carolina, Chapel Hill, North Carolina 27599 7090, USA
    Antioxid Redox Signal 4:769-81. 2002
    ....
  5. ncbi Dying a thousand deaths: redundant pathways from different organelles to apoptosis and necrosis
    John J Lemasters
    Department of Cell and Developmental Biology, University of North Carolina at Chapel Hill, 27599 7090, USA
    Gastroenterology 129:351-60. 2005
    ..This brief overview emphasizes the multiple and often redundant pathways between different organelles that lead ultimately to a cell's demise...
  6. ncbi Prevention of hepatic ischemia-reperfusion injury by green tea extract
    Zhi Zhong
    Department of Cell and Developmental Biology, University of North Carolina at Chapel Hill, 27599, USA
    Am J Physiol Gastrointest Liver Physiol 283:G957-64. 2002
    ..Therefore, GTE could prove to be effective in decreasing hepatic injury in disease states where ischemia-reperfusion occurs...
  7. ncbi Screening assays for the mitochondrial permeability transition using a fluorescence multiwell plate reader
    J R Blattner
    Department of Cell Biology and Anatomy, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7090, USA
    Anal Biochem 295:220-6. 2001
    ..This high-throughput multiwell assay is amenable for screening panels of compounds for their ability to promote or block the MPT...
  8. ncbi Role of the mitochondrial permeability transition in apoptotic and necrotic death after ischemia/reperfusion injury to hepatocytes
    J S Kim
    Department of Cell and Developmental Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 7090, USA
    Curr Mol Med 3:527-35. 2003
    ..Thus, apoptosis and necrosis after reperfusion share a common pathway, the MPT. Cell injury progressing to either necrosis or apoptosis by shared pathways can be more aptly termed necrapoptosis...
  9. ncbi Primary cirrhotic hepatocytes resist TGFbeta-induced apoptosis through a ROS-dependent mechanism
    Dalliah Black
    Division of Gastrointestinal Surgery, Department of Surgery, University of North Carolina, 320 Medical Wing E, Chapel Hill, NC 27599 7081, USA
    J Hepatol 40:942-51. 2004
    ..The purpose of this study was to determine if dysregulated hepatocyte growth occurs through deficient apoptosis...
  10. ncbi The mitochondrial permeability transition initiates autophagy in rat hepatocytes
    S P Elmore
    Department of Cell and Developmental Biology and Curriculum in Toxicology, University of North Carolina, Chapel Hill, NC 27599, USA
    FASEB J 15:2286-7. 2001
    ..In conclusion, the MPT initiates mitochondrial depolarization after autophagic stimulation and the subsequent sequestration of mitochondria into autophagosomes...
  11. ncbi NF-kappaB stimulates inducible nitric oxide synthase to protect mouse hepatocytes from TNF-alpha- and Fas-mediated apoptosis
    E Hatano
    Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA
    Gastroenterology 120:1251-62. 2001
    ..CONCLUSIONS: NO protects hepatocytes from TNF-alpha- and Fas-mediated apoptosis. Endogenous iNOS, which is activated by NF-kappaB via IKKbeta, provides partial protection from apoptosis...
  12. ncbi Gliotoxin-mediated apoptosis of activated human hepatic stellate cells
    Young Oh Kweon
    Division of Digestive Diseases and Nutrition, Department of Medicine, CB 7038, Glaxo Research Bldg Rm 156, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
    J Hepatol 39:38-46. 2003
    ..Gliotoxin induces apoptosis of activated human and rat HSCs by an unknown mechanism...
  13. ncbi Salicylate enhances necrosis and apoptosis mediated by the mitochondrial permeability transition
    Ki Wan Oh
    Department of Cell and Developmental Biology, University of North Carolina at Chapel Hill, 27599, USA
    Toxicol Sci 73:44-52. 2003
    ..Enhancement by salicylate of MPT-dependent apoptosis may play a role in protection by aspirin and other nonsteroidal anti-inflammatory drugs against colon, lung, and breast cancer...
  14. ncbi Mitochondrial permeability transition in the switch from necrotic to apoptotic cell death in ischemic rat hepatocytes
    Jae Sung Kim
    Department of Cell and Developmental Biology, School of Medicine, University of North Carolina, Chapel Hill, 27599, USA
    Gastroenterology 124:494-503. 2003
    ..Here, we investigated factors regulating how cell death switches from necrosis to apoptosis after ischemia/reperfusion injury...
  15. ncbi Glycine blocks opening of a death channel in cultured hepatic sinusoidal endothelial cells during chemical hypoxia
    Y Nishimura
    Department of Cell Biology and Anatomy, School of Medicine, University of North Carolina at Chapel Hill, 27599-7090, USA
    Cell Death Differ 8:850-8. 2001
    ..This metastable state culminates in non-specific breakdown of the plasma membrane permeability barrier and irreversible cell death...
  16. pmc Basal reactive oxygen species determine the susceptibility to apoptosis in cirrhotic hepatocytes
    Jay Raval
    Department of Surgery, University of North Carolina, Chapel Hill, NC 27599, USA
    Free Radic Biol Med 41:1645-54. 2006
    ..In conclusion, cirrhotic hepatocytes have a nonfocal distribution of ROS. However, normal and cirrhotic hepatocytes exhibit mitochondrial localization of ROS that is necessary for apoptosis...
  17. pmc Increased oxidative stress is associated with balanced increases in hepatocyte apoptosis and proliferation in glycerol-3-phosphate acyltransferase-1 deficient mice
    Linda E Hammond
    Department of Nutrition, CB 7461, 2301 Michael Hooker Research Building, Columbia Street, University of North Carolina, Chapel Hill, NC 27599, USA
    Exp Mol Pathol 82:210-9. 2007
    ..Thus, Gpat1-/- liver exhibits increased oxidative stress and sensitivity of the mitochondrial permeability transition pore, and a balanced increase in apoptosis and proliferation...
  18. ncbi Dependence of liver injury after hemorrhage/resuscitation in mice on NADPH oxidase-derived superoxide
    Mark Lehnert
    Department of Cell and Developmental Biology, University of North Carolina Chapel Hill, Chapel Hill, North Carolina 27599, USA
    Shock 19:345-51. 2003
    ..The absence of NADPH oxidase substantially attenuates hepatocellular injury after hemorrhagic shock and resuscitation, blunts neutrophil infiltration, and decreases formation of reactive oxygen and reactive nitrogen species...
  19. pmc Closure of VDAC causes oxidative stress and accelerates the Ca(2+)-induced mitochondrial permeability transition in rat liver mitochondria
    Andrey Tikunov
    Department of Cell and Developmental Biology, University of North Carolina at Chapel Hill, 27599, USA
    Arch Biochem Biophys 495:174-81. 2010
    ....
  20. ncbi Activated Kupffer cells cause a hypermetabolic state after gentle in situ manipulation of liver in rats
    P Schemmer
    Laboratory of Hepatobiology and Toxicology, Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA
    Am J Physiol Gastrointest Liver Physiol 280:G1076-82. 2001
    ..Thus modulation of Kupffer cell function before organ harvest could be beneficial in human liver transplantation and surgery...
  21. ncbi Liver regeneration is suppressed in small-for-size liver grafts after transplantation: involvement of c-Jun N-terminal kinase, cyclin D1, and defective energy supply
    Zhi Zhong
    Department of Cell and Developmental Biology, University of North Carolina, Chapel Hill, 29425, USA
    Transplantation 82:241-50. 2006
    ..Small-for-size liver grafts have decreased survival compared to full-size grafts. This study investigated mechanisms of suppression of liver regeneration in small-for-size grafts...
  22. ncbi Free radical-dependent dysfunction of small-for-size rat liver grafts: prevention by plant polyphenols
    Zhi Zhong
    Department of Cell and Developmental Biology, University of North Carolina, Chapel Hill, 27599, USA
    Gastroenterology 129:652-64. 2005
    ..The mechanisms by which small-for-size liver grafts decrease survival remain unclear. This study investigated the role of free radicals in injury to small-for-size grafts...
  23. ncbi Polyphenols from Camellia sinenesis prevent primary graft failure after transplantation of ethanol-induced fatty livers from rats
    Zhi Zhong
    Department of Cell and Developmental Biology, University of North Carolina, Chapel Hill, NC 27599, USA
    Free Radic Biol Med 36:1248-58. 2004
    ..In conclusion, polyphenols scavenged free radicals in ethanol-induced fatty livers and decreased injury after liver transplantation...
  24. ncbi Role of free radicals in failure of fatty liver grafts caused by ethanol
    Zhi Zhong
    Department of Cell and Developmental Biology, CB 7090, 236 Taylor Hall, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
    Alcohol 34:49-58. 2004
    ..Treatment of fatty donor livers with antioxidants and free radical scavengers may thus be an effective clinical therapy to prevent failure of fatty grafts...
  25. ncbi Hepatitis C virus core and nonstructural proteins induce fibrogenic effects in hepatic stellate cells
    Ramó Bataller
    Department of Medicine and Biochemistry and Biophysics, University of North Carolina at Chapel Hill 27599 7038, USA
    Gastroenterology 126:529-40. 2004
    ..Hepatocytes secrete HCV proteins, which may interact with hepatic stellate cells (HSCs). Our aims were to investigate whether HCV proteins induce fibrogenic effects on HSCs...
  26. ncbi Polyphenols from Camellia sinenesis attenuate experimental cholestasis-induced liver fibrosis in rats
    Zhi Zhong
    Dept of Cell and Developmental Biology, CB 7090, Univ of North Carolina at Chapel Hill, Chapel Hill, NC 27599 7090, USA
    Am J Physiol Gastrointest Liver Physiol 285:G1004-13. 2003
    ..Polyphenols from C. sinenesis scavenge oxygen radicals and prevent activation of stellate cells, thereby minimizing liver fibrosis...
  27. ncbi Effects of three superoxide dismutase genes delivered with an adenovirus on graft function after transplantation of fatty livers in the rat
    Thorsten G Lehmann
    Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 7038, USA
    Transplantation 76:28-37. 2003
    ..The purpose of this study was to identify the isoform with the highest effectiveness against ischemia/reperfusion injury after transplantation of fatty livers, which are particularly susceptible...
  28. ncbi L-Glycine: a novel antiinflammatory, immunomodulatory, and cytoprotective agent
    Zhi Zhong
    Departments of Cell and Developmental Biology, Pharmacology, Surgery and Environmental Health, University of North Carolina at Chapel Hill, North Carolina 27599 7090, USA
    Curr Opin Clin Nutr Metab Care 6:229-40. 2003
    ..This article will focus on the recent findings about the responsible mechanisms of protection and review the beneficial effects of glycine in different disease states...
  29. pmc Ethanol exposure decreases mitochondrial outer membrane permeability in cultured rat hepatocytes
    Ekhson Holmuhamedov
    Department of Cell and Developmental Biology, School of Medicine University of North Carolina at Chapel Hill, CB 7090, 236 Taylor Hall, Chapel Hill, NC 27599 7090, USA
    Arch Biochem Biophys 481:226-33. 2009
    ..Overall, these results demonstrate that acute ethanol exposure decreases mitochondrial outer membrane permeability most likely by inhibition of VDAC...
  30. ncbi Ischemic preconditioning of rat livers against cold storage-reperfusion injury: role of nonparenchymal cells and the phenomenon of heterologous preconditioning
    M Arai
    Department of Cell Biology and Anatomy, School of Medicine, University of North Carolina at Chapel Hill, USA
    Liver Transpl 7:292-9. 2001
    ..Moreover, ischemia to half the liver confers protection to the other half. Such heterologous preconditioning provides a new means to protect liver tissue against ischemia-reperfusion injury without imposing ischemia on the target tissue...
  31. ncbi Electrical properties and conduction in reperfused papillary muscle
    W E Cascio
    Department of Medicine, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 7075, USA
    Circ Res 89:807-14. 2001
    ....
  32. ncbi Mitochondrial permeability transition in acetaminophen-induced necrosis and apoptosis of cultured mouse hepatocytes
    Kazuyoshi Kon
    Department of Cell and Developmental Biology, University of North Carolina at Chapel Hill, 27599 7090, USA
    Hepatology 40:1170-9. 2004
    ..The MPT then induces ATP depletion-dependent necrosis or caspase-dependent apoptosis as determined, in part, by ATP availability from glycolysis...
  33. ncbi Roles of mitophagy and the mitochondrial permeability transition in remodeling of cultured rat hepatocytes
    Sara Rodriguez-Enriquez
    Department of Cell and Developmental Biology, University of North Carolina, Chapel Hill, NC, USA
    Autophagy 5:1099-106. 2009
    ..These findings indicate that mitochondrial autophagy (mitophagy) and the MPT underlie mitochondrial remodeling in cultured hepatocytes...
  34. ncbi Carolina rinse solution minimizes kidney injury and improves graft function and survival after prolonged cold ischemia
    Ming Yin
    Department of Cell and Developmental Biology, and Environmental Science and Engineering, University of North Carolina, Chapel Hill, North Carolina 27599, USA
    Transplantation 73:1410-20. 2002
    ..The purpose of this study was to determine whether Carolina rinse solution (CRS) used at the end of cold ischemic storage decreases kidney injury and improves graft function and survival...
  35. ncbi Discrimination of depolarized from polarized mitochondria by confocal fluorescence resonance energy transfer
    Steven P Elmore
    Department of Cell and Developmental Biology and Curriculum in Toxicology, University of North Carolina, Chapel Hill, NC 27599, USA
    Arch Biochem Biophys 422:145-52. 2004
    ..In conclusion, confocal FRET discriminates individual depolarized mitochondria against a background of hundreds of polarized mitochondria...
  36. pmc Transforming growth factor beta mediates hepatocyte apoptosis through Smad3 generation of reactive oxygen species
    Dalliah Black
    Department of Surgery, 4024 Burnett Womack Building, CB 7050, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
    Biochimie 89:1464-73. 2007
    ..In conclusion, TGFbeta-induced hepatocyte apoptosis occurs through Smad3 dependent activation of ROS with subsequent activation of the MPT and caspases...
  37. ncbi Mitochondrial permeability transition: a common pathway to necrosis and apoptosis
    Jae Sung Kim
    Department of Cell and Developmental Biology, University of North Carolina at Chapel Hill, CB 7090, 236 Taylor Hall, Chapel Hill, NC 27599 7090, USA
    Biochem Biophys Res Commun 304:463-70. 2003
    ..Thus, the MPT is a common pathway leading to both necrotic and apoptotic cell death after ischemia/reperfusion...
  38. ncbi Reduced-size liver transplantation in the mouse
    Lars O Conzelmann
    Department of Cell and Developmental Biology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 57599, USA
    Transplantation 76:496-501. 2003
    ..To investigate mechanisms underlying graft injury after RSLT, this study developed a model of RSLT in mice...
  39. ncbi Graft tumor necrosis factor receptor-1 protects after mouse liver transplantation whereas host tumor necrosis factor receptor-1 promotes injury
    Lars O Conzelmann
    Department of Cell and Developmental Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA, and Department of Trauma, Hand and Reconstructive Surgery, Hospitals of the J W Goethe University, Frankfurt, Germany
    Transplantation 82:1214-20. 2006
    ..TNFR1 mediates liver injury after ischemia/reperfusion but is also mitogenic during hepatic regeneration. This study investigated the role of graft and host TNFR1 in early graft injury after liver transplantation in mice...
  40. ncbi TRAIL-mediated apoptosis requires NF-kappaB inhibition and the mitochondrial permeability transition in human hepatoma cells
    Young Soo Kim
    Department of Medicine, University of North Carolina, Chapel Hill, NC, USA
    Hepatology 36:1498-508. 2002
    ..Inhibition of NF-kappaB unmasks a TRAIL-induced apoptotic signaling cascade that involves FADD, caspase 8, the MPT, and caspase 3...
  41. ncbi Nitric oxide protects rat hepatocytes against reperfusion injury mediated by the mitochondrial permeability transition
    Jae Sung Kim
    Department of Cell and Developmental Biology, School of Medicine, University of North Carolina, Chapel Hill, NC, USA
    Hepatology 39:1533-43. 2004
    ....
  42. ncbi Reactive oxygen species, but not Ca2+ overloading, trigger pH- and mitochondrial permeability transition-dependent death of adult rat myocytes after ischemia-reperfusion
    Jae Sung Kim
    Department of Cell and Developmental Biology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 7090, USA
    Am J Physiol Heart Circ Physiol 290:H2024-34. 2006
    ..In contrast, Ca2+ overloading appears to be the consequence of bioenergetic failure after the MPT and is not a factor promoting MPT onset...
  43. ncbi Tracker dyes to probe mitochondrial autophagy (mitophagy) in rat hepatocytes
    Sara Rodriguez-Enriquez
    Department of Cell and Developmental Biology, University of North Carolina, Chapel Hill, North Carolina 27599 7090, USA
    Autophagy 2:39-46. 2006
    ..The results show that mitochondria once selected for mitophagy are rapidly digested and support the concept that mitochondrial autophagy involves the MPT and signaling through PI3 kinase and possibly JNK...
  44. ncbi Differential requirement for c-Jun NH2-terminal kinase in TNFalpha- and Fas-mediated apoptosis in hepatocytes
    Robert F Schwabe
    Department of Medicine, University of North Carolina, Chapel Hill, North Carolina, USA
    FASEB J 18:720-2. 2004
    ..This study demonstrates that JNK augments TNF-alpha-induced apoptosis in hepatocytes through a signaling pathway that is distinct from the pathway by which it regulates proliferation...
  45. ncbi Regulated and unregulated mitochondrial permeability transition pores: a new paradigm of pore structure and function?
    Lihua He
    Department of Cell and Developmental Biology, University of North Carolina at Chapel Hill, CB 7090, 236 Taylor Hall, Chapel Hill, NC 27599 7090, USA
    FEBS Lett 512:1-7. 2002
    ..When protein clusters exceed chaperones available to block conductance, unregulated pore opening occurs...
  46. ncbi Different patterns of renal cell killing after warm and cold ischemia
    Ming Yin
    Department of Cell and Developmental Biology, University of North Carolina, Chapel Hill 27599 7090, USA
    Ren Fail 24:147-63. 2002
    ..In conclusion, warm ischemia triggers injury primarily to proximal tubular cells, whereas cold ischemia damages glomerular podocytes and peritubular endothelial cells in addition to proximal tubules...
  47. ncbi Cloning of a rat cDNA encoding a novel LIM domain protein with high homology to rat RIL
    H Wang
    Department of Cell Biology and Anatomy, School of Medicine, University of North Carolina at Chapel Hill 27599, USA
    Gene 165:267-71. 1995
    ..4 kb, whose level was significantly decreased during chemical hypoxia...
  48. ncbi Role of mitochondrial permeability transition pores in mitochondrial autophagy
    Sara Rodriguez-Enriquez
    Department of Cell and Developmental Biology, School of Medicine, University of North Carolina at Chapel Hill, CB 7090, 236 Taylor Hall, Chapel Hill, NC 27599 7090, USA
    Int J Biochem Cell Biol 36:2463-72. 2004
    ..The mitochondrial permeability transition is also associated with necrosis and apoptosis after a variety of stimuli. This review emphasizes the role of the mitochondrial permeability transition as a key event in mitochondrial autophagy...
  49. ncbi Minimizing oxidative stress by gene delivery of superoxide dismutase accelerates regeneration after transplantation of reduced-size livers in the rat
    Thorsten G Lehmann
    Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
    Liver Transpl 12:550-9. 2006
    ..In conclusion, overexpression of SOD1 in RSL prevents primary non-function of reduced-size liver grafts and accelerates liver regeneration...
  50. ncbi Dephosphorylation of the Rieske iron-sulfur protein after induction of the mitochondrial permeability transition
    Lihua He
    Department of Cell and Developmental Biology, University of North Carolina, Chapel Hill, NC 27599 7090, USA
    Biochem Biophys Res Commun 334:829-37. 2005
    ..These findings suggest that RISP may be part of MPT pores and that dephosphorylation of RISP may play a role in regulation of the MPT...
  51. ncbi Nitric oxide: a signaling molecule against mitochondrial permeability transition- and pH-dependent cell death after reperfusion
    Jae Sung Kim
    Department of Cell and Developmental Biology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 7090, USA
    Free Radic Biol Med 37:1943-50. 2004
    ..Thus, NO prevents pH-dependent cell killing after ischemia/reperfusion by a guanylyl cyclase/cGMP/protein kinase G signaling cascade that blocks the MPT...
  52. ncbi Voltage-dependent anion channel (VDAC) as mitochondrial governator--thinking outside the box
    John J Lemasters
    Department of Cell and Developmental Biology, University of North Carolina, CB 7090, 236 Taylor Hall, Chapel Hill, NC 27599, USA
    Biochim Biophys Acta 1762:181-90. 2006
    ..Overall, these considerations suggest that VDAC is a dynamic regulator, or governator, of global mitochondrial function both in health and disease...
  53. ncbi Extrahepatic cells contribute to the progenitor/stem cell response following reduced-size liver transplantation in mice
    Lars O Conzelmann
    Laboratory of Hepatobiology and Toxicology, Center for Alcohol Studies, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
    Exp Biol Med (Maywood) 232:571-80. 2007
    ..Reduced-size liver transplantation using GFP(+) transgenic mice supports the hypothesis that recipient-derived progenitor cells are present and may contribute to liver regeneration following transplantation...
  54. ncbi Heat shock suppresses the permeability transition in rat liver mitochondria
    Lihua He
    Department of Cell and Developmental Biology, University of North Carolina, Chapel Hill, North Carolina 27599 7090, USA
    J Biol Chem 278:16755-60. 2003
    ..These results indicate that heat shock causes resistance to opening of MPT pores, which may contribute to heat shock protection against cellular injury...
  55. ncbi Isolated mouse liver mitochondria are devoid of glucokinase
    Ernesto Bustamante
    Department of Cell and Developmental Biology, School of Medicine, University of North Carolina, Chapel Hill, NC 27599 7090, USA
    Biochem Biophys Res Commun 334:907-10. 2005
    ..Thus, functional linkage of glucokinase to mitochondrial metabolism and apoptotic signaling is unlikely to be mediated by the physical association of glucokinase with mitochondria...
  56. ncbi Inhibition of mitochondrial respiration as a source of adaphostin-induced reactive oxygen species and cytotoxicity
    Son B Le
    Department of Oncology, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA
    J Biol Chem 282:8860-72. 2007
    ....
  57. ncbi Mechanisms of hepatotoxicity
    Hartmut Jaeschke
    Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA
    Toxicol Sci 65:166-76. 2002
    ..Because of such diverse mechanisms, hepatotoxicity remains a major reason for drug withdrawal from pharmaceutical development and clinical use...
  58. ncbi Inhibition of the mitochondrial permeability transition by the nonimmunosuppressive cyclosporin derivative NIM811
    Peter C Waldmeier
    Nervous System Research, Novartis Pharma Ltd, Basel, Switzerland
    Mol Pharmacol 62:22-9. 2002
    ..We conclude that NIM811 is a useful alternative to PKF220-384 to investigate the role of the mitochondrial permeability transition in apoptotic and necrotic cell death...
  59. pmc Minocycline and N-methyl-4-isoleucine cyclosporin (NIM811) mitigate storage/reperfusion injury after rat liver transplantation through suppression of the mitochondrial permeability transition
    Tom P Theruvath
    Center for Cell Death, Injury and Regeneration, Medical University of South Carolina, Charleston, SC 29425, USA
    Hepatology 47:236-46. 2008
    ..05). Conclusion: Minocycline and NIM811 attenuated graft injury after rat liver transplantation and improved graft survival. Minocycline and/or NIM811 might be useful clinically in hepatic surgery and transplantation...
  60. doi Ischemic preconditioning prevents free radical production and mitochondrial depolarization in small-for-size rat liver grafts
    Hasibur Rehman
    Department of Pharmaceutical Sciences, Medical University of South Carolina, Charleston, SC 29425, USA
    Transplantation 85:1322-31. 2008
    ..This study tested whether IP attenuates injury of small-for-size liver grafts by preventing free radical production and mitochondrial dysfunction...
  61. pmc Mitochondrial permeability transition in liver ischemia and reperfusion: role of c-Jun N-terminal kinase 2
    Tom P Theruvath
    Center for Cell Death, Injury and Regeneration, Department of Pharmaceutical and Biomedical Sciences, Charleston, SC, USA
    Transplantation 85:1500-4. 2008
    ..In conclusion, JNK2 contributes to hepatocellular injury and death after I/R in association with increased mitochondrial dysfunction via the MPT...
  62. pmc Translocation of iron from lysosomes into mitochondria is a key event during oxidative stress-induced hepatocellular injury
    Akira Uchiyama
    Department of Pharmaceutical and Biomedical Sciences, Medical University of South Carolina, Charleston, SC 29425, USA
    Hepatology 48:1644-54. 2008
    ....
  63. ncbi Reduction of ciclosporin and tacrolimus nephrotoxicity by plant polyphenols
    Zhi Zhong
    Department of Pharmaceutical Sciences, Medical University of South Carolina, Charleston, SC 29425, USA
    J Pharm Pharmacol 58:1533-43. 2006
    ..Taken together, these results demonstrate that both CsA and tacrolimus stimulate free radical production in the kidney, most likely in tubular cells, and that polyphenols minimize nephrotoxicity by scavenging free radicals...
  64. ncbi Apoptosis and necrosis in the liver: a tale of two deaths?
    Harmeet Malhi
    Department of Medicine, Mayo Clinic College of Medicine, Rochester, MN, USA
    Hepatology 43:S31-44. 2006
    ....
  65. pmc Opioid receptor-independent protection of ischemic rat hepatocytes by morphine
    Jae Sung Kim
    Department of Surgery, University of Florida, Gainesville, FL 32610, USA
    Biochem Biophys Res Commun 351:958-64. 2006
    ..These results indicate that morphine prevents anoxia/reoxygenation injury to hepatocytes. Protective mechanisms are associated with the potassium channels and NO, but are independent of opioid receptor-mediated signaling...
  66. ncbi Acetaminophen-induced oxidant stress and cell injury in cultured mouse hepatocytes: protection by N-acetyl cysteine
    Mary Lynn Bajt
    Liver Research Institute, University of Arizona, College of Medicine, Tucson, Arizona 85724, USA
    Toxicol Sci 80:343-9. 2004
    ..Thus, AAP-induced oxidant stress precedes cell necrosis and, in cultured hepatocytes, the oxidant stress is involved in the propagation of cell injury...
  67. ncbi Rusty notions of cell injury
    John J Lemasters
    J Hepatol 40:696-8. 2004
  68. pmc NADPH oxidase signal transduces angiotensin II in hepatic stellate cells and is critical in hepatic fibrosis
    Ramon Bataller
    Department of Medicine, Columbia University College of Physicians and Surgeons, 622 West 168th Street, New York, New York 10032, USA
    J Clin Invest 112:1383-94. 2003
    ..Moreover, expression of smooth muscle alpha-actin and expression of TGF-beta1 were reduced in p47phox-/- mice. Thus, NADPH oxidase mediates the actions of Ang II on HSCs and plays a critical role in liver fibrogenesis...
  69. pmc Attenuation of acute rejection in a rat liver transplantation model by a liver-targeted dextran prodrug of methylprednisolone
    Anjaneya P Chimalakonda
    School of Pharmacy, Texas Tech University Health Sciences Center, Amarillo, TX 79106, USA
    Transplantation 81:678-85. 2006
    ..We investigated the effects of a novel liver-targeted dextran prodrug of MP (DMP) in an orthotopic rat liver transplantation (OLT) model...
  70. ncbi Lipopolysaccharide-binding protein modulates hepatic damage and the inflammatory response after hemorrhagic shock and resuscitation
    Mark Lehnert
    Medical Univ of South Carolina, 280 Calhoun St, PO Box 250140, Charleston, SC 29425, USA
    Am J Physiol Gastrointest Liver Physiol 291:G456-63. 2006
    ..An absence of LBP blunts hepatocellular injury with decreased neutrophil infiltration, oxidative stress, and c-Jun and ERK activation...
  71. ncbi Apoptosis versus oncotic necrosis in hepatic ischemia/reperfusion injury
    Hartmut Jaeschke
    Liver Research Institute, University of Arizona, College of Medicine, Room 6309, 1501 N Campbell Avenue, Tucson, Arizona, USA
    Gastroenterology 125:1246-57. 2003
    ..However, elucidation of critical cell death pathways under clinically relevant conditions will show potentially important therapeutic intervention strategies in hepatic ischemia/reperfusion injury...
  72. ncbi Role of pH in protection by low sodium against hypoxic injury in isolated perfused rat livers
    Mariapia Vairetti
    Department of Internal Medicine and Therapeutics, University of Pavia, Pavia, Italy
    J Hepatol 44:894-901. 2006
    ..The purpose of the present study was to characterize the role of Na+, pH and cellular swelling in the pathogenesis of hypoxic injury to rat livers...
  73. ncbi Targeted gene delivery to sinusoidal endothelial cells: DNA nanoassociate bearing hyaluronan-glycocalyx
    Yoshiyuki Takei
    Department of Gastroenterology, Juntendo University School of Medicine, Toky, Japan
    FASEB J 18:699-701. 2004
    ..Moreover, PLL-g-HA effectively stabilized DNA triplex formation. In conclusion, the new PLL-g-HA/DNA carrier system permits targeted transfer of exogenous genes selectively to the SECs...
  74. ncbi Cyclophilin D as a drug target
    Peter C Waldmeier
    Nervous System Research, Novartis Pharma Ltd, CH 4002 Basel, Switzerland
    Curr Med Chem 10:1485-506. 2003
    ..It might be a tougher challenge to obtain compounds specific for CYP D vs. other cyclophilins, and/or of small molecular weight, allowing brain penetration to make them suitable for treating neurodegenerative diseases...
  75. ncbi Mitochondrial bax translocation accelerates DNA fragmentation and cell necrosis in a murine model of acetaminophen hepatotoxicity
    Mary Lynn Bajt
    Department of Pharmacology, Toxicology, and Therapeutics, University of Kansas Medical Center, 3901 Rainbow Blvd, MS 1018, Kansas City, KS 66160, USA
    J Pharmacol Exp Ther 324:8-14. 2008
    ..However, the persistent oxidant stress and peroxynitrite formation in mitochondria may eventually trigger the permeability transition pore opening and release intermembrane proteins independently of Bax...
  76. ncbi Genetic manipulation of sinusoidal endothelial cells
    Yoshiyuki Takei
    Department of Gastroenterology, Juntendo University School of Medicine, Tokyo, Japan
    J Gastroenterol Hepatol 22:S68-72. 2007
    ..So, the PLL-g-HA/DNA system permits targeted delivery of exogenous nucleotide agents selectively to the liver SEC, providing a novel strategy for manipulation of SEC functions...
  77. pmc Selective degradation of mitochondria by mitophagy
    Insil Kim
    Center for Cell Death, Injury and Regeneration, Departments of Pharmaceutical Sciences and Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, SC 29425, USA
    Arch Biochem Biophys 462:245-53. 2007
    ..This review provides an overview of the process of mitophagy, the possible role of the mitochondrial permeability transition in mitophagy and the importance of mitophagy in turnover of dysfunctional mitochondria...
  78. ncbi Bid activates multiple mitochondrial apoptotic mechanisms in primary hepatocytes after death receptor engagement
    Yongge Zhao
    Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261, USA
    Gastroenterology 125:854-67. 2003
    ..We intended to study the mechanisms in intact hepatocytes so that findings could be made in a proper cellular context and would be more physiologically relevant...
  79. ncbi Nuclear translocation of endonuclease G and apoptosis-inducing factor during acetaminophen-induced liver cell injury
    Mary Lynn Bajt
    Liver Research Institute, University of Arizona, College of Medicine, Tucson, Arizona 85724, USA
    Toxicol Sci 94:217-25. 2006
    ....
  80. ncbi Role of apoptosis in acetaminophen hepatotoxicity
    Kazuyoshi Kon
    Department of Gastroenterology, Juntendo University School of Medicine, Tokyo, Japan
    J Gastroenterol Hepatol 22:S49-52. 2007
    ..In conclusion, acetaminophen induces the MPT and ATP-depletion-dependent necrosis or caspase-dependent apoptosis as determined, in part, by ATP availability from glycolysis...