John Lemasters

Summary

Affiliation: Medical University of South Carolina
Country: USA

Publications

  1. pmc Regulation of mitochondrial function by voltage dependent anion channels in ethanol metabolism and the Warburg effect
    John J Lemasters
    Center for Cell Death, Injury and Regeneration, Medical University of South Carolina, Charleston, SC 29425, USA
    Biochim Biophys Acta 1818:1536-44. 2012
  2. pmc Warburg revisited: regulation of mitochondrial metabolism by voltage-dependent anion channels in cancer cells
    Eduardo N Maldonado
    Center for Cell Death, Injury, and Regeneration, Medical University of South Carolina, Charleston, SC, USA
    J Pharmacol Exp Ther 342:637-41. 2012
  3. pmc Polyphenols of Camellia sinenesis decrease mortality, hepatic injury and generation of cytokines and reactive oxygen and nitrogen species after hemorrhage/resuscitation in rats
    Mark Lehnert
    Department of Pharmaceutical and Biomedical Sciences, Medical University of South Carolina, 280 Calhoun Street, Charleston, SC 29425, USA
    BMC Complement Altern Med 10:46. 2010
  4. ncbi request reprint Modulation of mitochondrial membrane permeability in pathogenesis, autophagy and control of metabolism
    John J Lemasters
    Department of Pharmaceutical Sciences, Medical University of South Carolina, Charleston, South Carolina 29425, USA
    J Gastroenterol Hepatol 22:S31-7. 2007
  5. pmc Mitochondrial calcium and the permeability transition in cell death
    John J Lemasters
    Center for Cell Death, Injury and Regeneration, Medical University of South Carolina, Charleston, SC 29425, USA
    Biochim Biophys Acta 1787:1395-401. 2009
  6. 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
  7. pmc Inhibition of the mitochondrial permeability transition by protein kinase A in rat liver mitochondria and hepatocytes
    Peter Pediaditakis
    Center for Cell Death, Injury and Regeneration, Department of Pharmaceutical and Biomedical Sciences, Medical University of South Carolina, Charleston, 29425, USA
    Biochem J 431:411-21. 2010
  8. pmc Inhibition of transforming growth factor-beta/Smad signaling improves regeneration of small-for-size rat liver grafts
    Zhi Zhong
    Department of Pharmaceutical and Biomedical Sciences, Medical University of South Carolina, Charleston, SC 29425, USA
    Liver Transpl 16:181-90. 2010
  9. ncbi request reprint 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
  10. pmc Activation of the oxygen-sensing signal cascade prevents mitochondrial injury after mouse liver ischemia-reperfusion
    Zhi Zhong
    Dept of Pharmaceutical Sciences, Medical Univ of South Carolina, 280 Calhoun St, PO Box 250140, Charleston, SC 29425, USA
    Am J Physiol Gastrointest Liver Physiol 295:G823-32. 2008

Research Grants

  1. MECHANISM/S OF ALCOHOL-INDUCED LIVER GRAFT FAILURE
    John Lemasters; Fiscal Year: 2000
  2. LIVER PRESERVATION FOR TRANSPLANTATION
    John J Lemasters; Fiscal Year: 2010
  3. Mechanisms of I/R Injury to Hepatocytes
    John J Lemasters; Fiscal Year: 2010
  4. LIVER PRESERVATION FOR TRANSPLANTATION
    John Lemasters; Fiscal Year: 2009
  5. Mechanisms of I/R Injury to Hepatocytes
    John Lemasters; Fiscal Year: 2009
  6. LIVER PRESERVATION FOR TRANSPLANTATION
    John Lemasters; Fiscal Year: 2007
  7. Mechanisms of I/R Injury to Hepatocytes
    John Lemasters; Fiscal Year: 2007
  8. Molecular Pathogenesis of Apoptosis in Liver Cells
    John Lemasters; Fiscal Year: 2005
  9. MECHANISM(S) OF ALCOHOL-INDUCED LIVER GRAFT FAILURE
    John Lemasters; Fiscal Year: 2005
  10. Conference on Mitochondria and Pathogenesis
    John Lemasters; Fiscal Year: 2002

Collaborators

  • Zhi Zhong
  • HARTMUT W JAESCHKE
  • Lee Graves
  • Craig D Albright
  • Ivan Rusyn
  • Arthur Cederbaum
  • Reza Mehvar
  • D Pessayre
  • Peter C Waldmeier
  • Jae Sung Kim
  • Lihua He
  • Kazuyoshi Kon
  • Insil Kim
  • Tom P Theruvath
  • Ting Qian
  • Peter Pediaditakis
  • Mary Lynn Bajt
  • Sara Rodriguez-Enriquez
  • Robert T Currin
  • Hasibur Rehman
  • Mark Lehnert
  • Akira Uchiyama
  • David A Brenner
  • Venkat K Ramshesh
  • Ming Yin
  • Eduardo N Maldonado
  • Robert Schoonhoven
  • Kenichi Ikejima
  • Linda E Hammond
  • Dalliah Black
  • Takashi Nitta
  • Kevin E Behrns
  • Suzanne Lyman
  • Anjaneya P Chimalakonda
  • Harmeet Malhi
  • Jay Raval
  • Thorsten G Lehmann
  • Ernesto Bustamante
  • Cathleen Cover
  • Tamara R Knight
  • Robert F Schwabe
  • Steven P Elmore
  • Young Oh Kweon
  • Ki Wan Oh
  • Yongge Zhao
  • Harold E Mekeel
  • Young Soo Kim
  • Xing Xi Peng
  • Ingo Marzi
  • Henrik Lind
  • Xun Zhang
  • Ekhson Holmuhamedov
  • Ronald P Mason
  • Henry D Connor
  • Anwar Farhood
  • Gary L Wright
  • Andrey Tikunov
  • Sumio Watanabe
  • Mark C Snoddy
  • Shailendra Giri
  • Richard A Rippe
  • Nobuhiro Sato
  • Yoshiyuki Takei
  • Kyoko Okumura
  • Tomonori Aoyama
  • Rosalind A Coleman
  • Scott D Doughman
  • Kumiko Arai
  • Steven M Watkins
  • Eiji Kobayashi
  • Jon A Weidanz
  • Dagmara Mohuczy
  • Gregory J Gores
  • Hartwig Bunzendahl
  • Imam H Shaik
  • Donald L Montgomery
  • Tom Luedde
  • R Jude Samulski
  • Justin H Nguyen
  • Abdellah Mansouri
  • Brian Herman
  • Shigetoshi Ohshima
  • Yoshiya Nishimura
  • Bernd Schnabl
  • Wen Xing Ding
  • Simon Watkins
  • Lars O Conzelmann
  • Olivia M Smutney
  • Gavin E Arteel
  • Xiao Ming Yin

Detail Information

Publications58

  1. pmc Regulation of mitochondrial function by voltage dependent anion channels in ethanol metabolism and the Warburg effect
    John J Lemasters
    Center for Cell Death, Injury and Regeneration, Medical University of South Carolina, Charleston, SC 29425, USA
    Biochim Biophys Acta 1818:1536-44. 2012
    ..This article is part of a Special Issue entitled: VDAC structure, function, and regulation of mitochondrial metabolism...
  2. pmc Warburg revisited: regulation of mitochondrial metabolism by voltage-dependent anion channels in cancer cells
    Eduardo N Maldonado
    Center for Cell Death, Injury, and Regeneration, Medical University of South Carolina, Charleston, SC, USA
    J Pharmacol Exp Ther 342:637-41. 2012
    ..In conclusion, tubulin-dependent closure of VDACs represents a new mechanism contributing to the suppression of mitochondrial metabolism in the Warburg phenomenon...
  3. pmc Polyphenols of Camellia sinenesis decrease mortality, hepatic injury and generation of cytokines and reactive oxygen and nitrogen species after hemorrhage/resuscitation in rats
    Mark Lehnert
    Department of Pharmaceutical and Biomedical Sciences, Medical University of South Carolina, 280 Calhoun Street, Charleston, SC 29425, USA
    BMC Complement Altern Med 10:46. 2010
    ..The Aim of this study was to test the hypothesis that green tea (Camellia sinenesis) extract containing 85% polyphenols decreases injury after H/R in rats by scavenging ROS and RNS...
  4. ncbi request reprint Modulation of mitochondrial membrane permeability in pathogenesis, autophagy and control of metabolism
    John J Lemasters
    Department of Pharmaceutical Sciences, Medical University of South Carolina, Charleston, South Carolina 29425, USA
    J Gastroenterol Hepatol 22:S31-7. 2007
    ..Thus, VDAC serves as a global regulator, or governator, of mitochondrial function. Understanding of how these mitochondrial membrane permeability changes are themselves regulated remains incomplete and requires future study...
  5. pmc Mitochondrial calcium and the permeability transition in cell death
    John J Lemasters
    Center for Cell Death, Injury and Regeneration, Medical University of South Carolina, Charleston, SC 29425, USA
    Biochim Biophys Acta 1787:1395-401. 2009
    ..Thus, the exact role of Ca(2+) for inducing the MPT and cell death depends on the particular biologic setting...
  6. 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...
  7. pmc Inhibition of the mitochondrial permeability transition by protein kinase A in rat liver mitochondria and hepatocytes
    Peter Pediaditakis
    Center for Cell Death, Injury and Regeneration, Department of Pharmaceutical and Biomedical Sciences, Medical University of South Carolina, Charleston, 29425, USA
    Biochem J 431:411-21. 2010
    ..In conclusion, PKA in liver cytosol activated by cGMP or cAMP acts directly on mitochondria to delay onset of the MPT and protect hepatocytes from cell death after ischaemia/reperfusion...
  8. pmc Inhibition of transforming growth factor-beta/Smad signaling improves regeneration of small-for-size rat liver grafts
    Zhi Zhong
    Department of Pharmaceutical and Biomedical Sciences, Medical University of South Carolina, Charleston, SC 29425, USA
    Liver Transpl 16:181-90. 2010
    ..Together, these data show that TGF-beta is responsible, at least in part, for the defective liver regeneration in small-for-size grafts by activating the Smad signaling pathway...
  9. ncbi request reprint 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...
  10. pmc Activation of the oxygen-sensing signal cascade prevents mitochondrial injury after mouse liver ischemia-reperfusion
    Zhi Zhong
    Dept of Pharmaceutical Sciences, Medical Univ of South Carolina, 280 Calhoun St, PO Box 250140, Charleston, SC 29425, USA
    Am J Physiol Gastrointest Liver Physiol 295:G823-32. 2008
    ..In conclusion, IR causes the MPT and mitochondrial dysfunction, leading to hepatocellular death. PHI prevents MPT onset and liver damage through an effect mediated partially by HO-1...
  11. doi request reprint 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...
  12. 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
    ....
  13. 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...
  14. pmc Mitochondrial degradation by autophagy (mitophagy) in GFP-LC3 transgenic hepatocytes during nutrient deprivation
    Insil Kim
    Center for Cell Death, Injury and Regeneration, Medical University of South Carolina, QF308 Quadrangle Bldg, 280 Calhoun St, P O Box 250140, Charleston, SC 29425, USA
    Am J Physiol Cell Physiol 300:C308-17. 2011
    ..After autophagosome formation, mitochondrial depolarization and vesicular acidification occur, and mitochondrial contents, including mtDNA, are degraded...
  15. pmc NIM811 (N-methyl-4-isoleucine cyclosporine), a mitochondrial permeability transition inhibitor, attenuates cholestatic liver injury but not fibrosis in mice
    Hasibur Rehman
    Department of Pharmaceutical and Biomedical, Sciences, Medical University of South Carolina, Charleston, SC 29425, USA
    J Pharmacol Exp Ther 327:699-706. 2008
    ..Taken together, NIM811 decreased cholestatic necrosis and apoptosis but did not block fibrosis, indicating that the MPT plays an important role in cholestatic cell death in vivo...
  16. 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...
  17. pmc Lysosomal iron mobilization and induction of the mitochondrial permeability transition in acetaminophen-induced toxicity to mouse hepatocytes
    Kazuyoshi Kon
    Departments of Pharmaceutical and Biomedical Sciences and Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina 29425, USA
    Toxicol Sci 117:101-8. 2010
    ..Disrupted lysosomes are the likely source of iron, and chelation of this iron decreases acetaminophen toxicity to hepatocytes...
  18. ncbi request reprint Imaging of mitochondrial polarization and depolarization with cationic fluorophores
    John J Lemasters
    Center for Cell Death, Injury and Regeneration, and Departments of Pharmaceutical Sciences and Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, SC 29425, USA
    Methods Cell Biol 80:283-95. 2007
  19. ncbi request reprint 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...
  20. ncbi request reprint 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...
  21. ncbi request reprint 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...
  22. ncbi request reprint 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...
  23. ncbi request reprint 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...
  24. ncbi request reprint 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...
  25. ncbi request reprint 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...
  26. 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...
  27. ncbi request reprint 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...
  28. 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...
  29. ncbi request reprint 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...
  30. 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...
  31. ncbi request reprint 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...
  32. ncbi request reprint 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...
  33. ncbi request reprint 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...
  34. 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...
  35. ncbi request reprint 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...
  36. ncbi request reprint 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...
  37. ncbi request reprint 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 request reprint 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...
  39. ncbi request reprint 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...
  40. ncbi request reprint 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 request reprint 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...
  42. ncbi request reprint 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...
  43. ncbi request reprint 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...
  44. ncbi request reprint 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...
  45. ncbi request reprint 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...
  46. ncbi request reprint 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...
  47. ncbi request reprint Rusty notions of cell injury
    John J Lemasters
    J Hepatol 40:696-8. 2004
  48. ncbi request reprint 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
    ....
  49. ncbi request reprint 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...
  50. ncbi request reprint Peroxynitrite-induced mitochondrial and endonuclease-mediated nuclear DNA damage in acetaminophen hepatotoxicity
    Cathleen Cover
    Liver Research Institute, College of Medicine, University of Arizona, Tucson, 85724, USA
    J Pharmacol Exp Ther 315:879-87. 2005
    ..In contrast, nDNA fragmentation after AAP overdose is not caused by caspase-activated DNase but most likely by other intracellular DNase(s), whose activation is dependent on the mitochondrial oxidant stress and peroxynitrite formation...
  51. ncbi request reprint 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...
  52. ncbi request reprint 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...
  53. ncbi request reprint 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...
  54. ncbi request reprint 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...
  55. ncbi request reprint 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...
  56. ncbi request reprint 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
    ....
  57. ncbi request reprint 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...
  58. ncbi request reprint 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...

Research Grants17

  1. MECHANISM/S OF ALCOHOL-INDUCED LIVER GRAFT FAILURE
    John Lemasters; Fiscal Year: 2000
    ..This information will ultimately increase the pool of usable liver grafts, decrease the need for retransplantation surgery and minimize postoperative complications. ..
  2. LIVER PRESERVATION FOR TRANSPLANTATION
    John J Lemasters; Fiscal Year: 2010
    ..The information gained from the proposed experiments will be useful for improving clinical outcomes of not only so-called marginal donor livers but of virtually every liver graft. ..
  3. Mechanisms of I/R Injury to Hepatocytes
    John J Lemasters; Fiscal Year: 2010
    ....
  4. LIVER PRESERVATION FOR TRANSPLANTATION
    John Lemasters; Fiscal Year: 2009
    ..The information gained from the proposed experiments will be useful for improving clinical outcomes of not only so-called marginal donor livers but of virtually every liver graft. ..
  5. Mechanisms of I/R Injury to Hepatocytes
    John Lemasters; Fiscal Year: 2009
    ....
  6. LIVER PRESERVATION FOR TRANSPLANTATION
    John Lemasters; Fiscal Year: 2007
    ..Further, the investigators will validate their findings in a clinically relevant model of rat liver transplantation. ..
  7. Mechanisms of I/R Injury to Hepatocytes
    John Lemasters; Fiscal Year: 2007
    ....
  8. Molecular Pathogenesis of Apoptosis in Liver Cells
    John Lemasters; Fiscal Year: 2005
    ..abstract_text> ..
  9. MECHANISM(S) OF ALCOHOL-INDUCED LIVER GRAFT FAILURE
    John Lemasters; Fiscal Year: 2005
    ..This work will develop mechanism-based strategies to increase the use of marginal fatty livers for transplantation in the clinic and save lives. ..
  10. Conference on Mitochondria and Pathogenesis
    John Lemasters; Fiscal Year: 2002
    ..The purpose of this conference is to bring together leading researchers studying mitochondrial dysfunction in many different disease settings to share ideas and recent research findings. ..
  11. LIVER PRESERVATION FOR TRANSPLANTATION
    John J Lemasters; Fiscal Year: 2010
    ..The information gained from the proposed experiments will be useful for improving clinical outcomes of not only so-called marginal donor livers but of virtually every liver graft. ..