microRNA‐132 inhibits cardiomyocyte apoptosis and myocardial remodeling in myocardial infarction by targeting IL‐1β

Abstract

The patients suffering from myocardial infarction (MI) undergo cardiac remodeling with the features of expanded myocardial infarct size and dilated left ventricle.Multiple microRNAs (miRNAs) are emerged as crucial modulators to participate in the remodeling process. This study is mainly intended to clarify the regulatory mechanism of miR-132 in the MI-induced myocardial remodeling. miR-132 low expression, while interleukin-1β (IL-1β) high expression was determined in MI by reverse-transcription quantitative polymerase chain reaction and ELISA assays. MI rats showed decreased cardiac function and increased cardiomyocyte apoptosis.Moreover, miR-132 and IL-1β levels were altered in cardiomyocytes to explore their role in MI, with levels of proapoptotic or antiapoptotic proteins in MI together with cardiac function indexes observed. In addition, upregulation of miR-132, decreased levels of Bax and Cleaved Caspase-3, increased left ventricular ejection fraction, left ventricular fractional shortening, the maximum rate of rise or decrease of left ventricular pressure (±dp/dt max ), and Bcl-2 level, which could be reversed by overexpressing IL-1β. All in all, miR-132 inhibits cardiomyocyte apoptosis so as to ameliorate myocardial remodeling in rats with MI through IL-1β downregulation. Thus, miR-132 is a potential candidate for the MI treatment.

Polystyrene and Polyethylene Microplastics Decrease Cell Viability and Dysregulate Inflammatory and Oxidative Stress Markers of MDCK and L929 Cells In Vitro

“…3 ), the increase in TNFα concomitant with a decrease in IL1β may be indicative of the mechanistic differences in how the cells react to the presence of the microplastics in their environment. Although the expression of both TNFα and IL1β can both be co-regulated by the NF-κB pathway downstream of toll-like receptors (TLRs) and the recognition of damage-associated or pathogen-associated molecular patterns (DAMPs and PAMPs, respectively) (Oeckinghaus and Ghosh 2009 ), the upregulation of one inflammatory gene and downregulation of the other may be due to changes in expression of co-transcription factors such as HIF1α or AP-1 (Roy et al 2016 ; Walmsley et al 2014 ; Wen and Ting 2013 ), or microRNAs (Li et al 2020b ; Shen et al 2020 ; Zhao et al 2020 ). However, previous studies have found diverse microplastic-induced inflammatory gene modulations, lending further credence to our findings (Choi et al 2021a ; Wu et al 2020 ).…”

Modified Taohong Siwu Decoction Improved Heart Function After Myocardial Infarction by Inhibiting Inflammatory Factor and Promoting Chemotactic and Pro-Angiogenic Factors

“…The interleukin-1 receptor antagonist inhibited apoptosis and remodeling in experimental acute MI [31]. miR-132 inhibited cardiomyocyte apoptosis and myocardial remodeling after MI through downregulating IL-1β [32]. Interestingly, we found that MTHSWD signi cantly increased the level of TNF-α, which is an important proin ammatory factor, in the infarcted myocardium.…”

MicroRNA-132 attenuated cardiac fibrosis in myocardial infarction-induced heart failure rats

“…Differences genes are targeted by miR-132 in some diseases as previous studies. It showed that miR-132 inhibits cardiomyocyte apoptosis, and ameliorates myocardial remodeling in rats with MI through IL-1β down-regulation [ 35 ]. miR-132 exhibited the protective impacts on H9C2 cells against oxygen and glucose deprivation-induced injury via targeting FOXO3A [ 36 ].…”