CT-1 mediated cardioprotection against ischaemic re-oxygenation injury is mediated by P13 kinase, Akt and MEK1/2 pathways

被引：38

作者：

Brar, BK

Stephanou, A

Pennica, D

Latchman, DS

机构：

[1] Inst Child Hlth, Med Mol Biol Unit, London WC1 1EH, England

[2] Genentech Inc Labs, Dept Mol Oncol, San Francisco, CA USA

来源：

CYTOKINE | 2001年 / 16卷 / 03期

关键词：

CT-1; PI3-kinase; ischaemia; cell survival; cardiac myocytes;

D O I：

10.1006/cyto.2001.0951

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Cardiotrophin-1 protects cardiac myocytes from ischaemic re-oxygenation (IR) injury. CT-1 activates MEK1/2,p42/44MAPK as well as the phosphatidylinositol (PI) 3-OH kinase (PI3) protein kinase B (PKB/Akt) pathway. In this study we investigate the signalling pathways that mediate the anti-apoptotic cell survival effect of CT-1 in IR. Dominant negative gene based inhibitors of MEK1/2, PI3-kinase and Akt inhibited CT-1 mediated cardioprotection in re-oxygenation as did chemical inhibitors of the PI3-kinase pathway. Hence the PI3-kinase/Akt pathway is required in addition to MEK1/2 to mediate CT-1 cardioprotection in IR. (C) 2001 Academic Press.

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收藏

页码：93 / 96

页数：4

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