Blood microRNA 202-3p associates with the risk of essential hypertension by targeting soluble ST2

• Published in: Bioscience reports Vol. 40; no. 5
• Main Authors: Li, Lu, Zhong, Danrong, Xie, Yudan, Yang, Xinlei, Yu, Zuozhong, Zhang, Dangui, Jiang, Xinghua, Wu, Yanqing, Wu, Fangqin
• Format: Journal Article
• Language: English
• Published: England Portland Press Ltd 29-05-2020
• Subjects: Aged; Angiotensin II - pharmacology; Biomarkers - blood; Blood Pressure; Cardiovascular System & Vascular Biology; Case-Control Studies; Circulating MicroRNA - blood; Circulating MicroRNA - genetics; Epigenetics; Essential Hypertension - blood; Essential Hypertension - diagnosis; Essential Hypertension - genetics; Essential Hypertension - physiopathology; Feedback, Physiological; Female; Gene Expression Regulation; Humans; Interleukin-1 Receptor-Like 1 Protein - blood; Interleukin-1 Receptor-Like 1 Protein - genetics; Leukocytes, Mononuclear - drug effects; Leukocytes, Mononuclear - metabolism; Male; MicroRNAs - blood; MicroRNAs - genetics; Middle Aged; Molecular Bases of Health & Disease; THP-1 Cells; miR-202-3p; essential hypertension; sST2
• ISSN: 0144-8463; 1573-4935
• DOI: 10.1042/BSR20200378

MicroRNA (miR)-202-3p has attracted a great deal of attention in the fields of oncology, gynecology, and metabolic disorders. However, its role in cardiovascular diseases remains to be clarified. We previously found that disruption of miR-202-3p mediated regulation of expression of soluble (s)ST2, a decoy receptor for interleukin (IL)-33, promotes essential hypertension (EH). In the present study, we first measured miR-202-3p expression levels in the blood of 182 EH cases and 159 healthy controls using TaqMan assays. miR-202-3p levels were shown to be significantly higher in EH cases than controls (fold change = 3.58, P<0.001). Logistic regression analysis revealed that higher miR-202-3p expression was associated with an increased occurrence of EH (adjusted odds ratio (OR): 1.57; 95% confidence interval (CI), 1.36-1.82; P<0.001). Addition of miR-202-3p to traditional risk factors showed an additive prediction value for EH. Further functional experiments indicated that miR-202-3p could be induced by angiotensin II (Ang II) and inhibited by Ang II-triggered soluble ST2 (sST2) expression in a negative feedback manner. Moreover, blood miR-202-3p levels were negatively correlated with sST2 expression in vivo. Our study shows that blood miR-202-3p levels were significantly associated with the occurrence of EH. These findings indicate that miR-202-3p exerts a protective role against EH by antagonizing the induction of sST2 by Ang II.