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Modulation of Angiotensin II Effects in Vascular Smooth Muscle Cells by microRNAs

Angiotensin II (AngII)‐mediated vascular smooth muscle cell (VSMC) dysfunction plays a key role in cardiovascular diseases. However, the role of microRNAs (miRNAs) in this process is unclear. We used small RNA deep sequencing to profile AngII‐regulated miRNAs and evaluated their role in rat VSMC. Bioinformatics analysis showed that the predicted targets of AngII‐responsive miRNAs can modulate biological processes relevant to cardiovascular diseases. Further studies showed time‐ and dose‐dependent upregulation of miR‐32 and miR‐212 cluster (miR‐132/212) by AngII. We identified phosphatase and tensin homolog (PTEN) as a novel target of miR‐132 and showed miR‐132 mediates monocyte chemoattractant protein‐1 (MCP‐1) induction in VSMC partly via PTEN repression. miR‐132 overexpression also enhanced cyclic AMP‐response element binding protein (CREB) phosphorylation whereas its inhibition attenuated AngII‐induced CREB activation. Furthermore, miR‐132 induction by AngII required CREB activation, demonstrating a positive feedback loop. Notably, aortas from AngII‐infused mice showed higher levels of miR‐132/212 and MCP‐1. In addition, microarray analysis combined with RT‐QPCR revealed that a subset of genes downregulated by AngII was miR‐132 predicted targets, and they are associated with AngII functions. These results suggest that miR132/212 fine‐tunes and amplifies AngII actions in VSMC.