Activated Akt protects the lung from oxidant-induced injury and delays death of mice

被引:77
作者
Lu, YB
Parkyn, L
Otterbein, LE
Kureishi, Y
Walsh, K
Ray, A
Ray, P
机构
[1] Yale Univ, Sch Med, Dept Internal Med, Pulm & Crit Care Sect, New Haven, CT 06520 USA
[2] Tufts Univ, Sch Med, Sackler Sch Biomed Sci, Program Cell Mol & Dev Biol, Boston, MA 02135 USA
[3] Tufts Univ, Sch Med, St Elizabeths Med Ctr, Div Cardiovasc Res, Boston, MA 02135 USA
关键词
hyperoxia; lung; Akt; apoptosis; survival;
D O I
10.1084/jem.193.4.545
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Oxidant-induced injury to the lung causes extensive damage to lung epithelial cells. Impaired protection and repair of the lung epithelium can result in death. The serine-threonine kinase Akt has been implicated in inhibiting cell death induced by different stimuli including growth factor withdrawal, cell cycle discordance, DNA damage, and loss of cell adhesion in different cell types. However, the in vivo relevance of this prosurvival pathway has not been explored. Here we show that a constitutively active form of Akt introduced intratracheally into the lungs of mice by adenovirus gene transfer techniques protects mice from hyperoxic pulmonary damage and delays death of mice. This is the first demonstration of the in vivo protective function of Akt in the context of oxidant-induced lung injury.
引用
收藏
页码:545 / 549
页数:5
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