Neuroglobin-overexpressing transgenic mice are resistant to cerebral and myocardial ischemia

被引：194

作者：

Khan, Adil A. ^{[1
]}

Wang, Yaoming ^{[1
]}

Sun, Yunjuan ^{[1
]}

Mao, Xiao Ou ^{[1
]}

Xie, Lin ^{[1
]}

Miles, Erin ^{[1
]}

Graboski, Justin ^{[1
]}

Chen, Sylvia ^{[1
]}

Ellerby, Lisa M. ^{[1
]}

Jin, Kunlin ^{[1
]}

Greenberg, David A. ^{[1
]}

机构：

[1] Buck Inst Age Res, Novato, CA 94945 USA

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2006年 / 103卷 / 47期

关键词：

enclothelial nitric oxide synthase; myocardial infarction; stroke;

D O I：

10.1073/pnas.0607497103

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Neuroglobin (Ngb), a protein related to myoglobin and hemoglobin but expressed predominantly in the brain, is induced by neuronal hypoxia and cerebral ischemia and protects against hypoxic or ischemic neuronal injury. We engineered transgenic mice that overexpress murine Ngb under the control of a chicken beta-actin promoter, resulting in enhanced Ngb expression in multiple cell types and multiple tissues, including brain and heart. In Ngb-overexpressing transgenic mice compared with wild-type littermates, the volume of cerebral infarcts after occlusion of the middle cerebral artery was reduced by approximate to 30%, and the volume of myocardial infarcts produced by occlusion of the left anterior descending coronary artery was reduced by approximate to 25%. Ngb overexpression was associated with enhanced expression of endothelial nitric oxide synthase in vascular endothelial cells. These findings extend prior evidence for cytoprotection by Ngb and suggest both direct (parenchymatous) and indirect (vasomotor) protective mechanisms.

引用

页码：17944 / 17948

页数：5

共 30 条

[1] Atypical neural messengers [J].