Abstract 528: MicroRNA-30 Family Inhibits Neointima Hyperplasia by Targeting CaMKIIδ
miRNA is one class of small and non-coding RNAs, which regulate coding gene expressions. miR-30 family members are abundantly expressed in the vascular smooth muscle layer in the artery walls. However, the roles of miR-30 in vascular smooth muscle and vascular diseases are little unknown. Here, we report that the expression of miR-30 family members is dramatically reduced in the vascular walls upon vascular injury. Rescuing down-regulated miR-30 by overexpression using lenti-vitral delivery in injured rat carotid artery significantly inhibited injury-induced neointima formation. In vitro, the expression of miR-30 family members in the dedifferentiated cultured vascular smooth muscle cells (VSMCs) was approximately 50% lower than it in the intact vascular smooth muscle. Western blot analysis and luciferase assay showed that miR-30 directly targeted 3' UTR of calcium calmodulin dependent protein kinase II δ isoform (CaMKIIδ) and inhibited CaMKIIδ expression in the culture VSMCs. VSMC proliferation was significantly inhibited by overexpressing miR-30 and this inhibitory effect was partially recovered by CaMKIIδ rescue. These data suggest that miR-30 is a strong and novel regulatory factor in neointima formation, and may be developed to be a new therapeutic target to prevent or reduce vascular diseases.
Author Disclosures: Y. Liu: None. H. Singer: None.
- © 2014 by American Heart Association, Inc.