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

被引：0
|
作者：
Wang, Jianzhong [1 ,2 ]
Ouyang, Chun [1 ,2 ,3 ]
Chen, Xiangmei [1 ,2 ]
Fu, Bo [1 ,2 ]
Lu, Yang [1 ,2 ]
Hong, Quan [1 ,2 ]
机构：
[1] Gen Hosp Chinese PLA, Kidney Inst, Beijing 100853, Peoples R China
[2] Gen Hosp Chinese PLA, Key Lab Chinese PLA, Dept Nephrol, Beijing 100853, Peoples R China
[3] Nanjing Med Univ, Affiliated Hosp 1, Dept Nephrol, Nanjing, Peoples R China
来源：
JOURNAL OF NEPHROLOGY | 2008年 / 21卷 / 06期
关键词：
Apoptosis; ATP depletion; Jak2 kinase inhibitor; Stat;
D O I：
暂无
中图分类号：
R5 [内科学]; R69 [泌尿科学（泌尿生殖系疾病）];
学科分类号：
1002 ; 100201 ;
摘要：
Background: 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.
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收藏
页码：919 / 923
页数：5
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