1. MicroRNA-221 regulates endothelial nitric oxide production and inflammatory response by targeting adiponectin receptor 1.
- Author
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Chen, Chao-Feng, Huang, Jinyu, Li, Hong, Zhang, Chu, Huang, Xurui, Tong, Guoxin, and Xu, Yi-Zhou
- Subjects
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MICRORNA , *ENDOTHELIAL cells , *NITRIC oxide , *ADIPONECTIN , *NF-kappa B - Abstract
Adiponectin exerts anti-atherosclerosis property through its 2 receptors (AdipoR1 and AdipoR2). The mechanism regulating the expression of adiponectin receptors is unclear. Bioinformatics analysis showed that miR-221 targeted the 3′-untranslated region (3′UTR) of the AdipoR1 mRNA. The protein level and the mRNA level of AdipoR1 were reduced when miR-221 was expressed in human umbilical vein endothelial cells (HUVECs). Meanwhile, miR-221 repressed the activity of luciferase reporter containing the 3′UTR of AdipoR1. The inhibitory effect of miR-221 was abolished when the miR-221 binding site within the AdipoR1 3′UTR was deleted. Overexpression of miR-221 inhibited adiponectin-stimulated nitric oxide (NO) production in HUVECs. Furthermore, miR-221 abolished the inhibitory effect of adiponectin on NF-kB activation and the expression of adhesion molecules. Altogether, these results indicated that miR-221 targets AdipoR1 to regulate endothelial inflammatory response. [ABSTRACT FROM AUTHOR]
- Published
- 2015
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