Omi / HtrA 2 protease is associated with tubular cell apoptosis and fibrosis induced by unilateral ureteral obstruction

Jinu Kim, Dong Sun Kim, Mae Ja Park, Hee-Jung Cho, Antonis S. Zervos, Joseph V. Bonventre, and Kwon Moo Park Department of Anatomy, Kyungpook National University School of Medicine, Daegu, Republic of Korea; Biomolecular Science Center, College of Medicine, University of Central Florida, Orlando, Florida; and Renal Division, Brigham and Women’s Hospital, Department of Medicine, Harvard Medical School, Boston, Massachusetts

[1]  K. Park,et al.  Reactive oxygen species differently regulate renal tubular epithelial and interstitial cell proliferation after ischemia and reperfusion injury. , 2010, American journal of physiology. Renal physiology.

[2]  K. Park,et al.  Reactive oxygen species/oxidative stress contributes to progression of kidney fibrosis following transient ischemic injury in mice. , 2009, American journal of physiology. Renal physiology.

[3]  Shanshan Yang,et al.  UCF‐101, A Novel Omi/HtrA2 Inhibitor, Protects Against Cerebral Ischemia/Reperfusion Injury in Rats , 2009, Anatomical record.

[4]  Jeen-Woo Park,et al.  Increased superoxide formation induced by irradiation preconditioning triggers kidney resistance to ischemia-reperfusion injury in mice. , 2009, American journal of physiology. Renal physiology.

[5]  Jeen-Woo Park,et al.  Role of cytosolic NADP+-dependent isocitrate dehydrogenase in ischemia-reperfusion injury in mouse kidney. , 2009, American journal of physiology. Renal physiology.

[6]  D. Poppas,et al.  A novel cell-permeable antioxidant peptide decreases renal tubular apoptosis and damage in unilateral ureteral obstruction. , 2008, American journal of physiology. Renal physiology.

[7]  K. Fukunaga,et al.  Activation of HtrA2, a mitochondrial serine protease mediates apoptosis: current knowledge on HtrA2 mediated myocardial ischemia/reperfusion injury. , 2008, Cardiovascular therapeutics.

[8]  Y. Boo,et al.  Wen‐pi‐tang‐Hab‐Wu‐ling‐san attenuates kidney fibrosis induced by ischemia/reperfusion in mice , 2008, Phytotherapy research : PTR.

[9]  P. Vandenabeele,et al.  The mitochondrial serine protease HtrA2/Omi: an overview , 2008, Cell Death and Differentiation.

[10]  K. Fukunaga,et al.  Inhibition of HtrA2/Omi ameliorates heart dysfunction following ischemia/reperfusion injury in rat heart in vivo. , 2007, European journal of pharmacology.

[11]  F. Dehghani,et al.  The serine protease Omi/HtrA2 is involved in XIAP cleavage and in neuronal cell death following focal cerebral ischemia/reperfusion , 2007, Neurochemistry International.

[12]  J. Downward,et al.  The protease inhibitor Ucf-101 induces cellular responses independently of its known target, HtrA2/Omi , 2006, Cell Death and Differentiation.

[13]  In Sup Kil,et al.  Orchiectomy Attenuates Post-ischemic Oxidative Stress and Ischemia/Reperfusion Injury in Mice , 2006, Journal of Biological Chemistry.

[14]  D. Rigamonti,et al.  Prevention of cytosolic IAPs degradation: a potential pharmacological target in Huntington's Disease. , 2005, Pharmacological research.

[15]  Guido Kroemer,et al.  Caspase-independent cell death , 2005, Nature Medicine.

[16]  K. Park,et al.  Acute renal failure in zebrafish: a novel system to study a complex disease. , 2005, American journal of physiology. Renal physiology.

[17]  A. Schimmer.  Inhibitor of Apoptosis Proteins: Translating Basic Knowledge into Clinical Practice , 2004, Cancer Research.

[18]  N. Cheong,et al.  Inhibitor of Apoptosis Proteins Are Substrates for the Mitochondrial Serine Protease Omi/HtrA2* , 2003, Journal of Biological Chemistry.

[19]  Jinyu Ren,et al.  Omi/HtrA2 catalytic cleavage of inhibitor of apoptosis (IAP) irreversibly inactivates IAPs and facilitates caspase activity in apoptosis. , 2003, Genes & development.

[20]  S. Srinivasula,et al.  Characterization of a Novel and Specific Inhibitor for the Pro-apoptotic Protease Omi/HtrA2* , 2003, The Journal of Biological Chemistry.

[21]  S. Klahr,et al.  Obstructive nephropathy and renal fibrosis. , 2002, American journal of physiology. Renal physiology.

[22]  K. Park,et al.  Prevention of Kidney Ischemia/Reperfusion-induced Functional Injury, MAPK and MAPK Kinase Activation, and Inflammation by Remote Transient Ureteral Obstruction* , 2002, The Journal of Biological Chemistry.

[23]  J. Downward,et al.  The Serine Protease Omi/HtrA2 Regulates Apoptosis by Binding XIAP through a Reaper-like Motif* , 2002, The Journal of Biological Chemistry.

[24]  Yuri Lazebnik,et al.  Identification of Omi/HtrA2 as a Mitochondrial Apoptotic Serine Protease That Disrupts Inhibitor of Apoptosis Protein-Caspase Interaction* , 2002, The Journal of Biological Chemistry.

[25]  H. Nakayama,et al.  A serine protease, HtrA2, is released from the mitochondria and interacts with XIAP, inducing cell death. , 2001, Molecular cell.

[26]  R. Takahashi,et al.  Ubiquitin-protein ligase activity of X-linked inhibitor of apoptosis protein promotes proteasomal degradation of caspase-3 and enhances its anti-apoptotic effect in Fas-induced cell death , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[27]  P. Vandenabeele,et al.  Inhibition of apoptosis induced by ischemia-reperfusion prevents inflammation. , 1999, The Journal of clinical investigation.

[28]  S. Korsmeyer,et al.  BCL-2 family members and the mitochondria in apoptosis. , 1999, Genes & development.

[29]  M. del Río,et al.  Partial ATP depletion induces Fas- and caspase-mediated apoptosis in MDCK cells. , 1999, American journal of physiology. Renal physiology.

[30]  J C Reed,et al.  IAP family proteins--suppressors of apoptosis. , 1999, Genes & development.

[31]  T. Inagami,et al.  Accelerated fibrosis and collagen deposition develop in the renal interstitium of angiotensin type 2 receptor null mutant mice during ureteral obstruction. , 1998, Kidney international.

[32]  K. Park,et al.  Reactive oxygen species generated by renal ischemia and reperfusion trigger protection against subsequent renal ischemia and reperfusion injury in mice. , 2010, American journal of physiology. Renal physiology.

[33]  K. Park,et al.  Original Article : Kidney Tubular Cell Regeneration Starts in the Deep Cortex after Ischemia , 2008 .

[34]  J. Fitzpatrick,et al.  Evidence that inhibition of tubular cell apoptosis protects against renal damage and development of fibrosis following ureteric obstruction. , 2006, American journal of physiology. Renal physiology.

[35]  H. Quesneville,et al.  Detection of New Transposable Element Families in Drosophila melanogaster and Anopheles gambiae Genomes , 2003, Journal of Molecular Evolution.