Inhibition of Nogo-B promotes cardiac hypertrophy via endoplasmic reticulum stress

Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie
J LiXiaojing Liu

Abstract

Nogo-B is a key endoplasmic reticulum (ER) protein that regulates ER stress signaling. However, its role in cardiac hypertrophy remains poorly understood. ER stress is interrelated with autophagy in the process of cardiac hypertrophy. Therefore, we aimed to test the hypothesis that both ER stress and autophagy signaling mediate the function of Nogo-B in cardiac hypertrophy. Rat models of transverse aortic constriction (TAC), neonatal rat cardiomyocytes (NRCMs) stimulated with norepinephrine (Ne) and primary cardiac fibroblasts treated with transforming growth factor β1 (TGF-β1) were used in this study. The expression of Nogo-B and markers of ER stress were determined by quantitative RT-PCR, western blotting and immunofluorescence. Autophagy was measured by monitoring autophagic flux. Specific small interfering RNA (siRNA) of Nogo-B was transfected to investigate the role of Nogo-B in regulating cardiac hypertrophy. In TAC-induced hypertrophic heart tissues, Ne-treated hypertrophic cardiomyocytes and TGF-β1-stimulated cardiac fibroblasts, the expression of Nogo-B, and markers of ER stress were significantly elevated. Impairment of autophagic flux was observed in the activated cardiac fibroblasts. Down-regulation of Nogo-B by siR...Continue Reading

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Citations

Jun 11, 2019·Oxidative Medicine and Cellular Longevity·Yanguo XinXiaojing Liu
May 13, 2020·Cardiovascular Drugs and Therapy·Xing ChenShiming Liu
Jun 23, 2020·Oxidative Medicine and Cellular Longevity·Junteng ZhouXiaojing Liu
Nov 27, 2020·Frontiers in Cell and Developmental Biology·Peng GaoZhiming Zhu
Feb 22, 2021·Journal of Cellular and Molecular Medicine·Wenhua LeiMao Chen

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