In this study, we found that mi R-16 was highly expressed in VSMCs and the expression level of mi R-16 was comparable to that of mi R-143 and mi R-145, two VSMC specific mi RNAs.Using lentiviral vector, we silenced the expression of mi R-16 in VSMCs and determined the functions of mi R-16 in VSMCs by studying VSMC growth and found that silencing mi R-16 in VSMCs promoted Ang II-induced cell proliferation, migration by promoting ERK1/2 and p38 cellular survival pathways.mi RNAs have been shown to regulate vascular smooth muscle cell (VSMC) function and play vital roles in hypertension, restenosis and atherosclerosis.
We previously identified the mi R-15a/16-1 cluster in rats, locating in chromosome 15, which is highly conserved among different mammalian species .
The mi R-15b/16-2 cluster locates in chromosome 3 in humans, 2 in rats and 3 in mice and is also highly conserved.
Moreover, silencing mi R-16 enhanced Ang II induced cell cycle associated gene expression and promoted Ang IIactivated cell proliferative pathways ERK1/2 and p38.
Our finding demonstrated for the first time that mi R-16 was a potential therapeutic target by participating in the Ang II-associated multiple signaling pathways in cardiovascular diseases.
Visit for more related articles at Cell & Developmental Biology mi RNAs are a class of non-coding endogenous small RNAs that control gene expression at the posttranscriptional level and involved in cell proliferation, migration and differentiation.