miR-487b mitigates chronic heart failure through inhibition of the IL-33/ST2 signaling pathway
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En-Wei Wang1, Xu-Sheng Jia1, Chang-Wu Ruan2 and Zhi-Ru Ge2
1Department of Cardiac Surgery, Linyi People's Hospital, Linyi 276003, China
2Department of Cardiology, Gongli Hospital Affiliated to Second Military Medical University, Shanghai 200135, China
Xu-Sheng Jia, email: email@example.com
Keywords: miR-487b, IL-33, ST2, chronic heart failure, signaling pathway
Received: November 02, 2016 Accepted: May 06, 2017 Published: June 07, 2017
We investigated the effects of microRNA-587b (miR-487b) in a rat model of chronic heart failure (CHF). Wistar rats were assigned to 10 groups (n=8 per group). Expression of interleukin-33 (IL-33), somatostatin 2 (ST2), IL-6, and TNF-α was higher in the CHF group than the control group. In the CHF, negative control (NC) for si-IL-33, NC for miR-487b mimic, NC for miR-487b inhibitor, and miR-487b inhibitor + si IL-33 groups, as compared to the blank and sham groups: steroid binding protein (SBP), D binding protein (DBP), left ventricular systolic pressure (LVSP), ± dp/dtmax, and superoxide dismutase (SOD) were all lower; myocardial fibrosis, MDA, left ventricular end-diastolic pressure (LVEDP), myocardial apoptosis rate, IL-6, and TNF-α were all higher; levels of IL-33 and ST2 mRNA and protein were higher; and levels of miR-487b were lower. Levels of IL-33 and ST2 mRNA and protein were lower, and SBP, DBP, LVSP, ± dp/dtmax, and SOD were higher in the miR-487b mimic and si-IL-33 groups than the CHF group. Expression of miR-487b was increased in the miR-487b mimic group, and expression of IL-33 and ST2 were increased and expression of miR-487b was decreased in the miR-487b inhibitor group. MiR-487b reduces apoptosis, inflammatory responses, and fibrosis in CHF by suppressing IL-33 through inhibition the IL-33/ST2 signaling pathway.
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