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Effect of Jak2 kinase inhibition on Stat1 and Stat3 activation and apoptosis of tubular epithelial cells induced by ATP depletion/recovery.

AbstractBACKGROUND:
Apoptosis is involved in acute renal failure (ARF). Its exact mechanism still remains to be explored. The Jak-Stat pathway participates in inflammation, apoptosis and tumorigenesis. In an in vitro model of renal ischemia/reperfusion injury (IRI), we investigated the role of Jak2 kinase inhibition on signal transducer and activator of transcription 1 (Stat1) and Stat3 activations as well as apoptosis of human proximal tubular epithelial cells (HKCs) induced by adenosine triphosphate (ATP) depletion/recovery.
METHODS:
ATP depletion of HKCs is induced by antimycin A.
RESULTS:
The Jak2-specific inhibitor AG490 decreased Stat1 and Stat3 phosphorylations and promoted HKC apoptosis induced by ATP depletion/recovery.
CONCLUSIONS:
Our results have demonstrated that Jak2 inhibition participated in the ATP depletion-induced apoptosis of HKCs, which might be a potential target for prevention and treatment of ARF.
AuthorsJianzhong Wang, Chun Ouyang, Xiangmei Chen, Bo Fu, Yang Lu, Quan Hong
JournalJournal of nephrology (J Nephrol) 2008 Nov-Dec Vol. 21 Issue 6 Pg. 919-23 ISSN: 1121-8428 [Print] Italy
PMID19034877 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Enzyme Inhibitors
  • STAT1 Transcription Factor
  • STAT1 protein, human
  • STAT3 Transcription Factor
  • STAT3 protein, human
  • Tyrphostins
  • alpha-cyano-(3,4-dihydroxy)-N-benzylcinnamide
  • Adenosine Triphosphate
  • Janus Kinase 2
Topics
  • Adenosine Triphosphate (metabolism)
  • Apoptosis (drug effects)
  • Blotting, Western
  • Cells, Cultured
  • Enzyme Inhibitors (pharmacology)
  • Epithelial Cells (drug effects, metabolism, pathology)
  • Humans
  • Janus Kinase 2 (antagonists & inhibitors)
  • Kidney Tubules, Proximal (metabolism, pathology)
  • STAT1 Transcription Factor (drug effects, metabolism)
  • STAT3 Transcription Factor (drug effects, metabolism)
  • Tyrphostins (pharmacology)

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