Minzhi Xu1, Ting Yu2. 1. Department of Cardiac Function, The Affiliated Hospital of Yangzhou University, 45 Taizhou Road, Yangzhou, 225001, Jiangsu, China. 2. Department of Cardiac Function, The Affiliated Hospital of Yangzhou University, 45 Taizhou Road, Yangzhou, 225001, Jiangsu, China. yuting_221@hotmail.com.
Abstract
INTRODUCTION: MicroRNAs (miRNAs), have been frequently reported to regulate various diseases including hypertension. However, the biological role and regulatory mechanism of miR-20b-5p are unclear in hypertension. The current study aimed to investigate the role of miR-20b-5p in hypertension. METHODS: Bioinformatics analysis (starBase: http://starbase.sysu.edu.cn ) and a wide range of experiments including blood pressure detection, morphometric sampling by electron microscopy, real-time quantitative polymerase chain reaction (RT-qPCR), CCK-8, western blot, luciferase reporter, hematoxylin and eosin (H&E) staining and Masson trichrome staining assays were used to explore the function and mechanism of miR-20b-5p in hypertension. RESULTS: MiR-20b-5p level was significantly upregulated in Spontaneously hypertensive rats' (SHRs') thoracic aortic vascular tissues. In function, miR-20b-5p silencing inhibited the proliferation and migration of aortic smooth muscle cells (ASMCs) of SHRs. In mechanism, we predicted 10 potential target mRNAs for miR-20b-5p. After prediction by bioinformatics, MAGI3 was validated to bind with miR-20b-5p. Rescue assays showed that MAGI3 silencing reversed the inhibitive influence of miR-20b-5p depletion on cell proliferation and migration. CONCLUSIONS: MiR-20b-5p contributed to the dysfunction of ASMCs by targeting MAGI3 in hypertension. This new discovery provided a potential novel insight for hypertension treatment.
INTRODUCTION: MicroRNAs (miRNAs), have been frequently reported to regulate various diseases including hypertension. However, the biological role and regulatory mechanism of miR-20b-5p are unclear in hypertension. The current study aimed to investigate the role of miR-20b-5p in hypertension. METHODS: Bioinformatics analysis (starBase: http://starbase.sysu.edu.cn ) and a wide range of experiments including blood pressure detection, morphometric sampling by electron microscopy, real-time quantitative polymerase chain reaction (RT-qPCR), CCK-8, western blot, luciferase reporter, hematoxylin and eosin (H&E) staining and Masson trichrome staining assays were used to explore the function and mechanism of miR-20b-5p in hypertension. RESULTS: MiR-20b-5p level was significantly upregulated in Spontaneously hypertensive rats' (SHRs') thoracic aortic vascular tissues. In function, miR-20b-5p silencing inhibited the proliferation and migration of aortic smooth muscle cells (ASMCs) of SHRs. In mechanism, we predicted 10 potential target mRNAs for miR-20b-5p. After prediction by bioinformatics, MAGI3 was validated to bind with miR-20b-5p. Rescue assays showed that MAGI3 silencing reversed the inhibitive influence of miR-20b-5p depletion on cell proliferation and migration. CONCLUSIONS: MiR-20b-5p contributed to the dysfunction of ASMCs by targeting MAGI3 in hypertension. This new discovery provided a potential novel insight for hypertension treatment.