Delayed cytoprotection induced by hypoxic preconditioning in cultured neonatal rat cardiomyocytes: Role of GRP78

Life Sciences ◽  
2007 ◽  
Vol 81 (13) ◽  
pp. 1042-1049 ◽  
Author(s):  
Yan-Xia Pan ◽  
An-Jing Ren ◽  
Juan Zheng ◽  
Wei-Fang Rong ◽  
Hong Chen ◽  
...  
1995 ◽  
Vol 76 (6) ◽  
pp. 1071-1078 ◽  
Author(s):  
Douwe E. Atsma ◽  
E.M. Lars Bastiaanse ◽  
Anastazia Jerzewski ◽  
Lizet J.M. Van der Valk ◽  
Arnoud Van der Laarse

1997 ◽  
Vol 121 (1) ◽  
pp. 118-124 ◽  
Author(s):  
Klaus Pönicke ◽  
Ingrid Heinroth-Hoffmann ◽  
Karin Becker ◽  
Otto-Erich Brodde

2018 ◽  
Vol 38 (2) ◽  
Author(s):  
Su Ming ◽  
Wang Shui-yun ◽  
Qiu Wei ◽  
Li Jian-hui ◽  
Hui Ru-tai ◽  
...  

Hypertrophic cardiomyopathy (HCM) is a serious monogenic disease characterized by cardiac hypertrophy, fibrosis, sudden cardiac death, and heart failure. Previously, we identified that miR-139-5p was down-regulated in HCM patients. However, the regulatory effects of miR-139-5p remain unclear. Thus, we investigated the role of miR-139-5p in the regulation of cardiac hypertrophy. The expression of miR-139-5p in left ventricular tissues in HCM patients and mice subjected to transverse aortic constriction (TAC) was significantly down-regulated. Knockdown of miR-139-5p expression in neonatal rat cardiomyocytes (NRCMs) induced cardiomyocyte enlargement and increased atrial natriuretic polypeptide (ANP) expression. Overexpression of miR-139-5p antagonized isoproterenol (ISO)-induced cardiomyocyte enlargement and ANP/brain natriuretic peptide (BNP) up-regulation. More importantly, we found that c-Jun expression was inhibited by miR-139-5p in NRCMs. Knockdown of c-Jun expression significantly attenuated cardiac hypertrophy induced by miR-139-5p deprivation. Our data indicated that miR-139-5p was down-regulated in the hearts of HCM patients and that it inhibited cardiac hypertrophy by targetting c-Jun expression.


1992 ◽  
Vol 21 (2) ◽  
pp. 87-100 ◽  
Author(s):  
Lula L. Hilenski ◽  
Ma Xuehui ◽  
Nancy Vinson ◽  
Louis Terracio ◽  
Thomas K. Borg

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