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.

引用

页码：919 / 923

页数：5

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