2. Academic Validation
  3. G protein-coupled receptor MAS1 induces an inhibitory effect on myocardial infarction-induced myocardial injury

G protein-coupled receptor MAS1 induces an inhibitory effect on myocardial infarction-induced myocardial injury

  • Int J Biol Macromol. 2022 May 15;207:72-80. doi: 10.1016/j.ijbiomac.2022.02.163.
Guo Zhou 1,  Leilei Fan 2,  Zhenzi Li 3,  Juan Li 4,  Xuejun Kou 4,  Ming Xiao 4,  Min Gao 4,  Xin Qu 4
Affiliations

Affiliations

  • 1 Second Department of Cardiology, Shandong Provincial Third Hospital, Cheeloo College of Medicine, Shandong University, Ji'nan 250031, Shandong, PR China. Electronic address: [email protected].
  • 2 First Department of Cardiology, Shandong Provincial Third Hospital, Cheeloo College of Medicine, Shandong University, Ji'nan 250031, Shandong, PR China. Electronic address: [email protected].
  • 3 Shandong Provincial Key Laboratory of Molecular Engineering, School of Chemistry and Chemical Engineering, Qilu University of Technology (Shandong Academy of Sciences), Ji'nan 250353, PR China.
  • 4 Second Department of Cardiology, Shandong Provincial Third Hospital, Cheeloo College of Medicine, Shandong University, Ji'nan 250031, Shandong, PR China.
PMID: 35247425 DOI: 10.1016/j.ijbiomac.2022.02.163
Abstract

Myocardial infarction (MI) is the most prevalent disease with high mortality, leading to devastating heart injury. Here, we aimed to explore the effect of MAS1 on the MI-induced myocardial injury. Significantly, we identified that the expression of MAS1 was decreased in the MI rat model and hypoxia and reoxygenation (H/R)-treated H9C2 cells. Hematoxylin & Eosin (H&E) staining revealed that the overexpression of MAS1 notably attenuated MI-related myocardium injury in the MI rat model. Echocardiography analysis revealed that MI inhibited left ventricular ejection fraction (LVEF) and left ventricular fraction shortening (LVFS), whereas the MAS1 overexpression could increase LVEF and LVFS in the MI rats. Meanwhile, the expression of collagen I, collagen III, α-SMA, ANP, and BNP was decreased by MAS1 overexpression in the MI rats. MAS1 attenuated cardiomyocyte Apoptosis in vivo and in vitro. Mechanically, the overexpression of MAS1 decreased the expression of PTEN and enhanced the phosphorylation of PI3K and Akt in vivo and in vitro. The overexpression of PTEN and the PI3K Inhibitor LY294002 could reverse the MAS1-mediated MI injury. Thus, we conclude that MAS1 inhibits MI-induced myocardial injury by modulating PTEN/PI3K/Akt signaling. Our finding provides new insight into the mechanism by which MAS1 attenuates MI-related cardiac dysfunction.

Keywords

MAS1; MI; Myocardial injury; PTEN/PI3K/AKT signaling.

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