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MiR-20a-5p overexpression prevented diabetic cardiomyopathy via inhibition of cardiomyocyte apoptosis, hypertrophy, fibrosis, and JNK/NF-κB signaling pathway.

Xiaoyu Liu,Bingyan Guo,Wei Zhang,Bocong Ma,Yongjun Li

Published 2021 in Journal of Biochemistry (Tokyo)

ABSTRACT

Diabetic cardiomyopathy (DCM) is a common cardiovascular disease. A declined miR-20a-5p was observed in hearts of diabetic mice, while its effect on DCM remains unknown. Herein, we established streptozotocin-induced DCM rat model and high glucose-stimulated H9C2 model of DCM. They then were treated with adenovirus expressing miR-20a-5p to explore the function of miR-20a-5p. ITT and ipGTT assay revealed that miR-20a-5p reduced blood glucose level. Besides, miR-20a-5p improved cardiac dysfunction reflected by reduced HW/BW and LVDP, and increased LVSP and ±LV dp/dt max. MiR-20a-5p prevented cardiomyocyte apoptosis, along with the up-regulated c-caspase-3, bax and down-regulated bcl-2. Moreover, miR-20a-5p alleviated cardiac hypertrophy as the parameters of ANP, BNP and MyHC-β decreased. Also, miR-20a-5p attenuated the cardiac fibrosis demonstrated by decreased TGF-β1, collagen I levels and the inflammatory response manifested by reduced IL-6, TNF-α and IL-1β production. Furthermore, miR-20a-5p prevented JNK phosphorylation and NF-κB p65nuclear translocation. Similarly, the effects of miR-20a-5p on DCM were confirmed in our in vitro experiments. Additionally, ROCK2 is a possible target gene of miR-20a-5p. ROCK2 overexpression reversed the protective effect of miR-20a-5p on DCM. Overall, miR-20a-5p may effectively ameliorate DCM through improving cardiac metabolism, and subsequently inhibiting inflammation, apoptosis, hypertrophy, fibrosis, and JNK/NF-κB pathway via modulating ROCK2.

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