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H2 relaxin ameliorates angiotensin II-induced endothelial dysfunction through inhibition of excessive mitochondrial fission.

Lei Gao,Yue Liu,Ying Wang,Wenjia Chen,Kelaier Yang,Jiawen Li,Bo Lv,Xin Zhang,Jinyu Chi,Na Liu,Xinhua Yin,Xiaohui Zhang

Published 2019 in Biochemical and Biophysical Research Communications - BBRC

ABSTRACT

The physiological function of endothelial cells plays an important role in maintaining normal cardiovascular function. Endothelial dysfunction induced by AngII (angiotensin II) is the pathological mechanism of occurrence and development of cardiovascular diseases. Human recombinant relaxin-2 (H2 relaxin), which has protective effect on cardiovascular functions, ameliorates damage to endothelial cells induced by angiotensin II (AngII) treatment. However, the exact mechanisms remain unclear. In this study, we researched the mechanisms of H2 relaxin inhibiting AngII-induced endothelial dysfunction from the protective effect of H2 relaxin on endothelial function though inhibiting excessive mitochondrial fission. Here, we found that H2 relaxin increased eNOS, SOD1 expression, inhibited excessive mitochondrial fission and decreased ROS level in HUVECs treated with AngII. However, overexpression of fission protein 1 (Fis1) prevented H2 relaxin from protecting against AngII-induced low eNOS, SOD1 expression, excessive mitochondrial fission and increased ROS level in HUVECs. Our study indicated that excessive mitochondrial fission could be a target for H2 relaxin to treat endothelial dysfunction in angiocardiopathy.

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