HOME HELP CONTACT US SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by Li, Z. Articles by Ge, Z. Search for Related Content PubMed PubMed Citation Articles by Li, Z. Articles by Ge, Z.

Department of Cardiology, Qilu Hospital of Shandong University, Key Laboratory of Cardiovascular Remodeling and Function Research, Ministry of Education and Ministry of Health, Jinan 250012, China¹ Department of Orthopedic, Jinan Central Hospital, Medical School of Shandong University, Jinan, Shandong Province 250012, China² Department of Cardiology, Qingdao's Municipal Hospital, Qingdao, Shandong Province 266021, China

(Correspondence should be addressed to Z Ge; Email: gezhiming{at}sdu.edu.cn)

^* (Z Li and T Zhang contributed equally to this work)

Apoptosis plays a critical role in the diabetic cardiomyopathy, and endoplasmic reticulum stress (ERS) is one of the intrinsic apoptosis pathways. Previous studies have shown that the endoplasmic reticulum becomes swollen and dilated in diabetic myocardium, and ERS is involved in heart failure and diabetic kidney. This study is aimed to demonstrate whether ERS is induced in myocardium of streptozotocin (STZ)-induced diabetic rats. We established a type 1 diabetic rat model, used echocardiographic evaluation, hematoxylin–eosin staining, and the terminal deoxynucleotidyl transferase-mediated DNA nick-end labeling staining to identify the existence of diabetic cardiomyopathy and enhanced apoptosis in the diabetic heart. We performed immunohistochemistry, western blot, and real-time PCR to analyze the hallmarks of ERS that include glucose-regulated protein 78, CCAAT/enhancer-binding protein homologous protein (CHOP) and caspase12. We found these hallmarks to have enhanced expression in protein and mRNA levels in diabetic myocardium. Also, another pathway that can lead to cell death of ERS, c-Jun NH₂-terminal kinase-dependent pathway, was also activated in diabetic heart. Those results suggested that ERS was induced in STZ-induced diabetic rats' myocardium, and ERS-associated apoptosis occurred in the pathophysiology of diabetic cardiomyopathy.

This article has been cited by other articles:

				T. Miki, T. Miura, H. Hotta, M. Tanno, T. Yano, T. Sato, Y. Terashima, A. Takada, S. Ishikawa, and K. Shimamoto Endoplasmic Reticulum Stress in Diabetic Hearts Abolishes Erythropoietin-Induced Myocardial Protection by Impairment of Phospho-Glycogen Synthase Kinase-3{beta}-Mediated Suppression of Mitochondrial Permeability Transition Diabetes, December 1, 2009; 58(12): 2863 - 2872. [Abstract] [Full Text] [PDF]