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Perturbed ER homeostasis by IGF-IIR α promotes cardiac damage under stresses
In this study, we investigate the molecular mechanism and contribution of IGF-IIRα in endoplasmic reticulum stress induction in the heart under doxorubicin-induced cardiotoxicity. Using in vitro H9c2 cells, in vivo transgenic rat cardiac tissues, siRNAs against CHOP, chemical ER chaperone PBA, and western blot experiments, we found that IGF-IIRα overexpression enhanced ER stress markers ATF4, ATF6, IRE1α, and PERK which were further aggravated by DOX treatment. This was accompanied by a significant perturbation in stress-associated MAPKs such as p38 and JNK. Interestingly, PARKIN, a stress responsive cellular protective...
Source: Molecular and Cellular Biochemistry - September 29, 2021 Category: Biochemistry Authors: Sudhir Pandey Chia-Hua Kuo William Shao-Tsu Chen Yu-Lan Yeh Wei-Wen Kuo Ray-Jade Chen Cecilia Hsuan Day Pei-Ying Pai Tsung-Jung Ho Chih-Yang Huang Source Type: research

Gelsolin (GSN) induces cardiomyocyte hypertrophy and BNP expression via p38 signaling and GATA-4 transcriptional factor activation.
In this study, we used H9c2 and H9c2-GSN stable clones in an attempt to understand the mechanisms of GSN overexpression in cardiomyocytes. These data showed that the overexpression of GSN in H9c2-induced cardiac hypertrophy and increased the pathological hypertrophy markers atrial natriuretic peptide brain natriuretic peptide. Furthermore, we found that E-cadherin expression decreased with the overexpression of GSN in H9c2, but β-catenin expression increased. These data presume that the cytoskeleton is loose. Further, previous studies show that the mitogen-activated protein kinase pathway can induce cardiac hypertrophy. O...
Source: Molecular and Cellular Biochemistry - February 7, 2014 Category: Biochemistry Authors: Hu WS, Ho TJ, Pai P, Chung LC, Kuo CH, Chang SH, Tsai FJ, Tsai CH, Jie YC, Liou YM, Huang CY Tags: Mol Cell Biochem Source Type: research