Hong Pyo Kim

Summary

Affiliation: University of Pittsburgh
Country: USA

Publications

  1. ncbi request reprint CO as a cellular signaling molecule
    Hong Pyo Kim
    Department of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA
    Annu Rev Pharmacol Toxicol 46:411-49. 2006
  2. pmc Deletion of caveolin-1 protects against oxidative lung injury via up-regulation of heme oxygenase-1
    Yang Jin
    Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
    Am J Respir Cell Mol Biol 39:171-9. 2008
  3. ncbi request reprint The heme oxygenase-1/carbon monoxide pathway suppresses TLR4 signaling by regulating the interaction of TLR4 with caveolin-1
    Xiao Mei Wang
    Division of Pulmonary, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA
    J Immunol 182:3809-18. 2009
  4. pmc FLIP protects against hypoxia/reoxygenation-induced endothelial cell apoptosis by inhibiting Bax activation
    Xue Wang
    Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Pittsburgh Medical Center, 3459 Fifth Ave, MUH NW 628, Pittsburgh, PA 15213, USA
    Mol Cell Biol 25:4742-51. 2005
  5. ncbi request reprint FLIP inhibits endothelial cell apoptosis during hyperoxia by suppressing Bax
    Xue Wang
    Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Pittsburgh Medical Center, 3459 Fifth Avenue, MUH 628NW, Pittsburgh, PA 15213, USA
    Free Radic Biol Med 42:1599-609. 2007
  6. pmc Caveolin-1: a critical regulator of lung fibrosis in idiopathic pulmonary fibrosis
    Xiao Mei Wang
    Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA
    J Exp Med 203:2895-906. 2006
  7. pmc Carbon monoxide prevents ventilator-induced lung injury via caveolin-1
    Alexander Hoetzel
    Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA, USA
    Crit Care Med 37:1708-15. 2009
  8. doi request reprint Caveolin-1 regulates the secretion and cytoprotection of Cyr61 in hyperoxic cell death
    Yang Jin
    Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
    FASEB J 23:341-50. 2009
  9. ncbi request reprint Carbon monoxide protects against hyperoxia-induced endothelial cell apoptosis by inhibiting reactive oxygen species formation
    Xue Wang
    Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania 15213, USA
    J Biol Chem 282:1718-26. 2007
  10. ncbi request reprint Heat shock protein-70 mediates the cytoprotective effect of carbon monoxide: involvement of p38 beta MAPK and heat shock factor-1
    Hong Pyo Kim
    Department of Medicine, Division of Pulmonary, Allergy, and Critical Care Medicine, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA
    J Immunol 175:2622-9. 2005

Detail Information

Publications32

  1. ncbi request reprint CO as a cellular signaling molecule
    Hong Pyo Kim
    Department of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA
    Annu Rev Pharmacol Toxicol 46:411-49. 2006
    ..In this review, we summarize recent findings of the beneficial or detrimental effects of endogenous CO with an emphasis on the signaling pathways and downstream targets that trigger the action of this gas...
  2. pmc Deletion of caveolin-1 protects against oxidative lung injury via up-regulation of heme oxygenase-1
    Yang Jin
    Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
    Am J Respir Cell Mol Biol 39:171-9. 2008
    ..These studies identify caveolin-1 as a novel component involved in hyperoxia-induced lung injury...
  3. ncbi request reprint The heme oxygenase-1/carbon monoxide pathway suppresses TLR4 signaling by regulating the interaction of TLR4 with caveolin-1
    Xiao Mei Wang
    Division of Pulmonary, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA
    J Immunol 182:3809-18. 2009
    ..Upon LPS stimulation, HO-1 trafficked to the caveolae by a p38 MAPK-dependent mechanism, where it down-regulated proinflammatory signaling. These results reveal an anti-inflammatory network involving cav-1 and HO-1...
  4. pmc FLIP protects against hypoxia/reoxygenation-induced endothelial cell apoptosis by inhibiting Bax activation
    Xue Wang
    Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Pittsburgh Medical Center, 3459 Fifth Ave, MUH NW 628, Pittsburgh, PA 15213, USA
    Mol Cell Biol 25:4742-51. 2005
    ..The inhibitory effects of FLIP on Bax activation and plasma membrane DISC formation may play significant roles in protecting endothelial cells from the lethal effects of hypoxia/reoxygenation...
  5. ncbi request reprint FLIP inhibits endothelial cell apoptosis during hyperoxia by suppressing Bax
    Xue Wang
    Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Pittsburgh Medical Center, 3459 Fifth Avenue, MUH 628NW, Pittsburgh, PA 15213, USA
    Free Radic Biol Med 42:1599-609. 2007
    ..In conclusion, FLIP exerted novel inhibitory effects on extrinsic and intrinsic apoptotic pathways, which significantly protected endothelial cells from the lethal effects of hyperoxia...
  6. pmc Caveolin-1: a critical regulator of lung fibrosis in idiopathic pulmonary fibrosis
    Xiao Mei Wang
    Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA
    J Exp Med 203:2895-906. 2006
    ..This study indicates a pivotal role for cav-1 in ECM regulation and suggests a novel therapeutic target for patients with pulmonary fibrosis...
  7. pmc Carbon monoxide prevents ventilator-induced lung injury via caveolin-1
    Alexander Hoetzel
    Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA, USA
    Crit Care Med 37:1708-15. 2009
    ..We sought to determine the role of caveolin-1 in lung susceptibility to VILI in mice. Furthermore, we assessed the role of caveolin-1 in the tissue-protective effects of CO in the VILI model...
  8. doi request reprint Caveolin-1 regulates the secretion and cytoprotection of Cyr61 in hyperoxic cell death
    Yang Jin
    Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
    FASEB J 23:341-50. 2009
    ..Taken together, Cav-1/Cyr61 interaction via integrins represents a novel pathway of Cyr61 signaling involving cav-1-dependent processes, which play a critical role in regulating hyperoxia-induced cell death...
  9. ncbi request reprint Carbon monoxide protects against hyperoxia-induced endothelial cell apoptosis by inhibiting reactive oxygen species formation
    Xue Wang
    Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania 15213, USA
    J Biol Chem 282:1718-26. 2007
    ..We also show that carbon monoxide promoted an interaction of heme oxygenase-1 with Bax. These results define novel mechanisms underlying the antiapoptotic effects of carbon monoxide during hyperoxic stress...
  10. ncbi request reprint Heat shock protein-70 mediates the cytoprotective effect of carbon monoxide: involvement of p38 beta MAPK and heat shock factor-1
    Hong Pyo Kim
    Department of Medicine, Division of Pulmonary, Allergy, and Critical Care Medicine, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA
    J Immunol 175:2622-9. 2005
    ..These data provide a novel mechanism for the protective effects of CO and underscore a potential application of this gaseous molecule in anti-inflammatory therapies...
  11. ncbi request reprint Bcl-XL disrupts death-inducing signal complex formation in plasma membrane induced by hypoxia/reoxygenation
    Xue Wang
    Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania 15213, USA
    FASEB J 18:1826-33. 2004
    ..The inhibitory effects of Bcl-X(L) on DISC formation may play significant roles in protecting endothelial cells from H/R-induced cell death...
  12. ncbi request reprint Autophagic proteins regulate cigarette smoke-induced apoptosis: protective role of heme oxygenase-1
    Hong Pyo Kim
    Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh, MUH 628NW, Pittsburgh, Pennsylvania, USA
    Autophagy 4:887-95. 2008
    ..An understanding of the regulation of cell death pathways during smoke exposure may provide therapeutic strategies in smoke-related illness...
  13. pmc Identifying targets for COPD treatment through gene expression analyses
    Zhi Hua Chen
    Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, PA, USA
    Int J Chron Obstruct Pulmon Dis 3:359-70. 2008
    ..These studies have shed new light on the molecular mechanisms of COPD, and suggest novel targets for clinical treatments...
  14. pmc Mitochondrial localization and function of heme oxygenase-1 in cigarette smoke-induced cell death
    Dirk Jan Slebos
    Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, MUH 628NW, 3459 Fifth Ave, Pittsburgh, PA 15213, USA
    Am J Respir Cell Mol Biol 36:409-17. 2007
    ..We demonstrate the functional compartmentalization of heme oxygenase-1 in the mitochondria of lung epithelial cells, and its potential role in defense against mitochondria-mediated cell death during CSE exposure...
  15. pmc Caveolin-1 confers antiinflammatory effects in murine macrophages via the MKK3/p38 MAPK pathway
    Xiao Mei Wang
    Division of Pulmonary, Allergy, and Critical Care Medicine, University of Pittsburgh School of Medicine, 3459 Fifth Avenue, MUH 628, Pittsburgh, PA 15213, USA
    Am J Respir Cell Mol Biol 34:434-42. 2006
    ..Taken together, our data suggest that caveolin-1 acts as a potent immunomodulatory effector molecule in immune cells and that the regulation of LPS-induced cytokine production by caveolin-1 involves the MKK3/p38 MAPK pathway...
  16. pmc Caveolin-1 expression by means of p38beta mitogen-activated protein kinase mediates the antiproliferative effect of carbon monoxide
    Hong Pyo Kim
    Division of Pulmonary, Allergy, and Critical Care Medicine, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA
    Proc Natl Acad Sci U S A 102:11319-24. 2005
    ..Thus, we demonstrate that CO, by activating p38beta MAPK, up-regulates caveolin-1, which acts as a tumor suppressor protein that mediates the growth inhibitory properties of this gas...
  17. doi request reprint Analyzing autophagy in clinical tissues of lung and vascular diseases
    Hong Pyo Kim
    Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
    Methods Enzymol 453:197-216. 2009
    ..This chapter provides protocols for the isolation of distinct lung cell types, such as epithelial, endothelial, macrophages, and fibroblasts; as well as protocols for the analysis of autophagy in lung cells and tissues...
  18. pmc Carbon monoxide protects against ventilator-induced lung injury via PPAR-gamma and inhibition of Egr-1
    Alexander Hoetzel
    Department of Pulmonary, Allergy, and Critical Care Medicine, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA
    Am J Respir Crit Care Med 177:1223-32. 2008
    ..Ventilator-induced lung injury (VILI) leads to an unacceptably high mortality. In this regard, the antiinflammatory properties of inhaled carbon monoxide (CO) may provide a therapeutic option...
  19. ncbi request reprint Mechanisms of cell death in oxidative stress
    Stefan W Ryter
    Department of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, The University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, USA
    Antioxid Redox Signal 9:49-89. 2007
    ..Among these, the heme oxygenase-1/carbon monoxide system has emerged as a major intracellular antiapoptotic mechanism...
  20. pmc Carbon monoxide differentially inhibits TLR signaling pathways by regulating ROS-induced trafficking of TLRs to lipid rafts
    Kiichi Nakahira
    Division of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA
    J Exp Med 203:2377-89. 2006
    ..Thus, CO negatively controlled TLR signaling pathways by inhibiting translocation of TLR to lipid rafts through suppression of NADPH oxidase-dependent ROS generation...
  21. pmc Egr-1 regulates autophagy in cigarette smoke-induced chronic obstructive pulmonary disease
    Zhi Hua Chen
    Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
    PLoS ONE 3:e3316. 2008
    ..Autophagy is a degradative process involving lysosomal turnover of cellular components, though its role in human diseases remains unclear...
  22. pmc Transforming growth factor-β1 suppression of endotoxin-induced heme oxygenase-1 in macrophages involves activation of Smad2 and downregulation of Ets-2
    Su Wol Chung
    Division of Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women s Hospital and Harvard Medical School, Boston, Massachusetts, USA
    J Cell Physiol 227:351-60. 2012
    ..These data suggest that the return of HO-1 to basal levels during the resolution of an inflammatory response may involve its downregulation by anti-inflammatory mediators...
  23. ncbi request reprint Protective functions of heme oxygenase-1 and carbon monoxide in the respiratory system
    Stefan W Ryter
    Department of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, The University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, USA
    Antioxid Redox Signal 9:2157-73. 2007
    ..This review summarizes recent findings on the functions of heme oxygenase-1 in the respiratory system, with an emphasis on possible roles in disease progression and therapies...
  24. ncbi request reprint Heat-shock proteins: new keys to the development of cytoprotective therapies
    Hong Pyo Kim
    University of Pittsburgh, Division of Pulmonary Allergy and Critical Care Medicine, Department of Medicine, MUH 628NW, 3459 Fifth Avenue, Pittsburgh, PA 15213, USA
    Expert Opin Ther Targets 10:759-69. 2006
    ..Therefore, induction of cellular stress tolerance by preconditioning (e.g., heat shock) might be potential therapeutic targets...
  25. ncbi request reprint Caveolae compartmentalization of heme oxygenase-1 in endothelial cells
    Hong Pyo Kim
    Division of Pulmonary, Allergy, and Critical Care Medicine, Dept of Medicine, MUH 628NW, 3459 Fifth Ave, Pittsburgh, PA, 15213, USA
    FASEB J 18:1080-9. 2004
    ..We demonstrate for the first time the localization of heme degradation enzymes to plasma membrane caveolae, and present novel evidence that caveolin-1 interacts with and modulates HO activity...
  26. ncbi request reprint Cyr61 protects against hyperoxia-induced cell death via Akt pathway in pulmonary epithelial cells
    Yang Jin
    Division of Pulmonary, Allergy and Critical Care Medicine, 628 NW MUH, University of Pittsburgh Medical Center, 3459 5th Ave, Pittsburgh, PA 15213, USA
    Am J Respir Cell Mol Biol 33:297-302. 2005
    ..Taken together, our data demonstrate that Cyr61 expression provides cytoprotection in hyperoxia-induced pulmonary epithelial cell death and that this effect was in part mediated via the Akt signaling pathway...
  27. ncbi request reprint Hepatocyte growth factor protects against hypoxia/reoxygenation-induced apoptosis in endothelial cells
    Xue Wang
    Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania 15213, USA
    J Biol Chem 279:5237-43. 2004
    ..The inhibition of Bid/Bax-induced cell death by hepatocyte growth factor primarily involved p38 MAPK and in part Akt-dependent pathways but not ERK1/ERK2...
  28. ncbi request reprint Caveolin-1 stops profibrogenic signaling?
    Hong Pyo Kim
    Am J Physiol Lung Cell Mol Physiol 294:L841-2. 2008
  29. ncbi request reprint Evidence for heme oxygenase-1 association with caveolin-1 and -2 in mouse mesangial cells
    Nam Hee Jung
    Department of Pharmacology and Toxicology, College of Medicine, Inha University, Incheon, Korea
    IUBMB Life 55:525-32. 2003
    ..Co-localization of caveolins with HO-1 in caveolae suggested that caveolin could also play an important role in regulating the function of HO-1...
  30. ncbi request reprint A Peptide with anti-transglutaminase activity decreases lipopolysaccharide-induced lung inflammation in mice
    Gee Young Suh
    Department of Medicine, Division of Pulmonary and Critical Care Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea
    Exp Lung Res 32:43-53. 2006
    ..05). These results indicate that TGase may be a new therapeutic target in LPS-induced lung inflammation...
  31. ncbi request reprint A new road to induce heme oxygenase-1 expression by carbon monoxide
    Hong Pyo Kim
    Circ Res 101:862-4. 2007
  32. ncbi request reprint Down-regulation of organic anion transporter 2 mRNA expression by nitric oxide in primary cultured rat hepatocytes
    Seok Ho Cha
    Nitric Oxide Radical Toxicology Research Center, College of Medicine, Inha University, Incheon, Korea
    IUBMB Life 54:129-35. 2002
    ..Combined, our results suggest that rOAT2 mRNA expression in hepatocytes is down-regulated by NO at least at the transcriptional step...