miR-30e-5p Alleviates Inflammation and Cardiac Dysfunction After Myocardial Infarction Through Targeting PTEN
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ORIGINAL ARTICLE
miR-30e-5p Alleviates Inflammation and Cardiac Dysfunction After Myocardial Infarction Through Targeting PTEN Yongli Chen,1 Yan Yin,2 and Hua Jiang
1,3
(Received June 29, 2020; accepted October 25, 2020)
Abstract— Accumulating studies show that microRNAs are candidate biomarkers and ther-
apeutic targets for cardiovascular diseases including myocardial infarction (MI). Bioinformatics analysis suggested that compared with Sprague-Dawley (SD) rats without MI, miR30e-5p expression in the left ventricle tissue of SD rats with MI was significantly downregulated, suggesting miR-30e-5p may participate in the pathogenesis of MI. In this study, H9c2 cardiomyocytes were exposed to hypoxia to establish a hypoxic cell model. SD rats with left anterior descending coronary artery ligation were used for the MI animal model. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to evaluate the miR-30e-5p and PTEN mRNA expressions in cells and tissues. Western blot was used for detecting the expression of PTEN protein. miR-30e-5p expression in H9c2 cells was then inhibited or overexpressed, and its effects on viability and apoptosis were examined by cell counting kit-8 (CCK-8) assay and TUNEL assay, respectively. ELISA was used to detect inflammatory factors. The regulatory relationship between PTEN and miR-30e-5p was investigated by bioinformatics analysis, qRT-PCR, Western blot, and dual-luciferase reporter assay. It was found that miR-30e-5p expression was significantly downregulated in animal models and H9c2 cells under hypoxia. Overexpression of miR-30e-5p led to a dramatic increase of cell viability, accompanied by the decrease of IL-1β, TNF-α, IL-6, LDH, CK-MB, and cTnI. Furthermore, PTEN was identified as a target of miR-30e-5p, and PTEN overexpression reversed the effects of miR-30e -5p on H9c2 cells. To conclude, we confirm that miR-30e-5p alleviates inflammation and myocardial injury induced by MI via suppressing PTEN. KEY WORDS: miR-30e-5p; PTEN; myocardial infarction.
1
Department of Cardiology, Tianjin Chest Hospital, 261 Taierzhuang South Road, Jinnan District, Tianjin, 300222, China 2 Department of Respiratory, Tianjin Chest Hospital, Tianjin, 300222, China 3 To whom correspondence should be addressed at Department of Cardiology, Tianjin Chest Hospital, 261 Taierzhuang South Road, Jinnan District, Tianjin, 300222, China. E-mail: [email protected]
INTRODUCTION Although the prognosis of patients with myocardial infarction (MI) has been continuously improved, MI is still one of the leading causes of death and disability in
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Chen, Yin, and Jiang the world [1–3]. It is of great importance to explore possible novel therapeutic targets for MI. MicroRNAs (miRNAs) regulate gene expression by inhibiting translation or inducing degradation of target mRNAs. An increasing number of miRNAs are validated to be abnormally expressed in the development of MI. These miRNAs affect multiple biol
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