c-Jun N-terminal protein kinase signaling pathway mediates cardiac myocyte apoptosis in mouse congestive heart failure after myocardial infraction via endoplasmic reticulum stress

陈鹏; 杨成明; 曾春雨; 王旭开; 熊秀勤; 何多芬

您当前的位置：

首页 >

文章列表页 >

c-Jun N-terminal protein kinase signaling pathway mediates cardiac myocyte apoptosis in mouse congestive heart failure after myocardial infraction via endoplasmic reticulum stress

更新时间：2026-01-09

- c-Jun N-terminal protein kinase signaling pathway mediates cardiac myocyte apoptosis in mouse congestive heart failure after myocardial infraction via endoplasmic reticulum stress
- Journal of Army Medical University Vol. 31, Issue 24, Pages: 2455-2458(2009)
- 作者机构：
- 作者简介：
- 基金信息：
- DOI：
  CLC： R329.28;R363.21;R542.22
- Published：2009
- 稿件说明：
移动端阅览
陈鹏,杨成明,曾春雨,王旭开,熊秀勤,何多芬.JNK信号途径通过内质网应激反应介导心肌梗死后心力衰竭小鼠心肌组织的凋亡[J].陆军军医大学学报(原第三军医大学学报),2009,31(24):2455-2458.

　CHEN Peng,YANG Cheng-ming,ZENG Chun-yu,WANG Xu-kai,XIONG Xiu-qin,HE Duo-fen.c-Jun N-terminal protein kinase signaling pathway mediates cardiac myocyte apoptosis in mouse congestive heart failure after myocardial infraction via endoplasmic reticulum stress[J].J Amry Med Univ (J Third Mil Med Univ),2009,31(24):2455-2458.
陈鹏,杨成明,曾春雨,王旭开,熊秀勤,何多芬.JNK信号途径通过内质网应激反应介导心肌梗死后心力衰竭小鼠心肌组织的凋亡[J].陆军军医大学学报(原第三军医大学学报),2009,31(24):2455-2458. DOI：

　CHEN Peng,YANG Cheng-ming,ZENG Chun-yu,WANG Xu-kai,XIONG Xiu-qin,HE Duo-fen.c-Jun N-terminal protein kinase signaling pathway mediates cardiac myocyte apoptosis in mouse congestive heart failure after myocardial infraction via endoplasmic reticulum stress[J].J Amry Med Univ (J Third Mil Med Univ),2009,31(24):2455-2458. DOI：

摘要

目的探讨在心肌梗死后心力衰竭诱导的内质网应激反应中c-Jun氨基端激酶（c-Jun N-terminal kinase

JNK）通路介导心肌细胞凋亡可能的作用及机制。方法结扎小鼠左冠状动脉主干建立心肌梗死后心力衰竭（心衰）模型，32只小鼠采用随机数字法分4组：假手术组、心肌梗死后2、4、6周组，采用超声心动图观察心室扩张及心功能变化情况，Western blot检测内质网分子伴侣GRP78蛋白以及JNK蛋白及其磷酸化水平的表达。采用TUNEL法观察心肌细胞的凋亡情况。结果与假手术组相比较，心肌梗死后心力衰竭的小鼠左心室扩大，心功能下降。小鼠心肌组织GRP78表达明显增高（P0.05），JNK蛋白表达没有明显变化，但其活化形式磷酸化JNK表达增高（P0.05）。TUNEL染色显示心肌梗死后心力衰竭的小鼠心肌组织凋亡明显增多（P0.05）。结论心肌梗死后心力衰竭诱导内质网应激反应，并激活JNK信号途径促进了心肌细胞的凋亡。

Abstract

Objective To explore the contribution of the c-Jun N-terminal protein kinase (JNK) signaling pathway to cardiac myocyte apoptosis in mouse congestive heart failure due to myocardial infraction. Methods The mouse heart failure model was induced by acute myocardial infarction through ligating the left coronary artery. Thirty-two health male mice were randomly divided into 4 groups: sham operated group

2-week postoperative group

4-week postoperative group and 6-week postoperative group. The ventricular dilatation and left ventricular function were assessed by echocardiography. The expressions of GRP78

JNK and phosphorylated JNK were assessed by Western blot assay. The cardiac myocyte apoptosis were assessed by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL). Results Compared with the sham group

cardiac expression of endoplasmic reticulum chaperones GRP78 and phosphorylated JNK were significantly up-regulated in the operation groups (P0.05). The number of TUNEL positive cells were markedly increased in the operation group compared with the sham group (P0.05). Conclusion These findings suggest that the CNK signaling pathway partly mediates cardiac myocyte apoptosis in mouse congestive heart failure due to myocardial infraction via endoplasmic reticulum stress.

关键词

Keywords

references

Views

下载量

CSCD

Alert me when the article has been cited

提交

Tools

Publicity Resources

Effect of cinnamaldehyde on Bax/Bak and apoptosis of vascular endothelial cells in diabetic ulcers

Excessive mechanical stretch stress induces tendon cell apoptosis via mechanosensitive ion channel protein Piezo1

Defective hippocampal astrocyte and neuronal primary cilia function in offspring brain of pregnant rats with advanced age might be associated with promoting apoptosis through LKB1/AMPK pathway

Combined exposure to noise and CO induces adverse male reproductive effects in rats

Effect of polystyrene microplastics on apoptosis of male germ cells

Related Author

JIN Zheyu

XIE Chenlei

FAN Xinqi

YANG Shu

DONG Ruiyi

BAI Yanyu

DING Yarong

ZHOU Zhongzhi

Related Institution

Hunan Provincial Key Laboratory of Vascular Biology and Translational Medicine， Hunan University of Chinese Medicine

Department of Burn Wounds and Plastic Surgery， First Affiliated Hospital of Hunan University of Chinese Medicine

Department of Neurology Children’s Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Pediatrics

⁰