MiR-22-3p Suppresses Vascular Remodeling and Oxidative Stress by Targeting CHD9 during the Development of Hypertension

• Published in: Journal of vascular research Vol. 58; no. 3; pp. 180 - 190
• Main Authors: Chen, Hanqing, Xu, Xiru, Liu, Zhengqing, Wu, Yong
• Format: Journal Article
• Language: English
• Published: Basel, Switzerland S. Karger AG 01.05.2021
• Subjects: Animals; Aorta, Thoracic - metabolism; Aorta, Thoracic - pathology; Aorta, Thoracic - physiopathology; Cadherins - genetics; Cadherins - metabolism; Care and treatment; Cell Movement; Cell Proliferation; Development and progression; Disease Models, Animal; Gene Expression Regulation; Genetic aspects; Health aspects; Hypertension; Hypertension - genetics; Hypertension - metabolism; Hypertension - pathology; Hypertension - physiopathology; Methods in Vascular Biology; MicroRNA; MicroRNAs - genetics; MicroRNAs - metabolism; Muscle, Smooth, Vascular - metabolism; Muscle, Smooth, Vascular - physiopathology; Myocytes, Smooth Muscle - metabolism; Myocytes, Smooth Muscle - pathology; Neovascularization; Oxidative Stress; Rats; Rats, Inbred SHR; Rats, Sprague-Dawley; Signal Transduction; Vascular Remodeling; China; Hypertension; Oxidative stress; MiR-22-3p; Chromodomain helicase DNA-binding 9
• ISSN: 1018-1172; 1423-0135; 1423-0135
• DOI: 10.1159/000514311

Hypertension is considered a risk factor for a series of systematic diseases. Known factors including genetic predisposition, age, and diet habits are strongly associated with the initiation of hypertension. The current study aimed to investigate the role of miR-22-3p in hypertension. In this study, we discovered that the miR-22-3p level was significantly decreased in the thoracic aortic vascular tissues and aortic smooth muscle cells (ASMCs) of spontaneously hypertensive rats. Functionally, the overexpression of miR-22-3p facilitated the switch of ASMCs from the synthetic to contractile phenotype. To investigate the underlying mechanism, we predicted 11 potential target mRNAs for miR-22-3p. After screening, chromodomain helicase DNA-binding 9 (CHD9) was validated to bind with miR-22-3p. Rescue assays showed that the co-overexpression of miR-22-3p and CHD9 reversed the inhibitory effect of miR-22-3p mimics on cell proliferation, migration, and oxidative stress in ASMCs. Finally, miR-22-3p suppressed vascular remodeling and oxidative stress in vivo. Overall, miR-22-3p regulated ASMC phenotype switch by targeting CHD9. This new discovery provides a potential insight into hypertension treatment.