Effect of endoplasmic reticulum stress on cardiac myocyte apoptosis in mouse congestive heart failure induced by myocardial infraction / 中国病理生理杂志
Chinese Journal of Pathophysiology
;
(12)1989.
Article
in Chinese
| WPRIM
| ID: wpr-534159
ABSTRACT
AIM:
To explore the effect of endoplasmic reticulum stress on cardiac myocyte apoptosis in mouse congestive heart failure induced by myocardial infraction.METHODS:
The mouse model of heart failure was established by ligating the left anterior descending coronary to produce acute myocardial infarction.Thirty-two mice were divided into 4 groups sham group and groups of post-operation at time points of 2,4 or 6 weeks,respectively.The ventricular dilatation and left ventricular functions were assessed by echocardiography.The expression of GRP78,CHOP,caspase-12,cleaved caspase-12,JNK and phosphorylated-JNK was detected by Western blotting.The cardiac myocyte apoptosis was determined by terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labeling(TUNEL).RESULTS:
The cardiac expression of endoplasmic reticulum chaperones GRP78 was significantly increased in the hearts with functional failure.The upregulated expression of CHOP,phosphorylated-JNK and cleaved caspase-12 illuminated that the CHOP-JNK-caspase-12 dependent pathways for endoplasmic reticulum-initiated apoptosis were activated in the heart with functional failure by myocardial infraction.CONCLUSION:
These findings suggest that the congestive heart failure induced by myocardial infraction is associated with endoplasmic reticulum stress and activation of CHOP,JNK,caspase-12 dependent pathways for endoplasmic reticulum-initiated apoptosis.
Full text:
Available
Index:
WPRIM (Western Pacific)
Type of study:
Prognostic study
Language:
Chinese
Journal:
Chinese Journal of Pathophysiology
Year:
1989
Type:
Article
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