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Background  Earlier, we reported that the simultaneous exposure of pulmonary arterial smooth muscle cells to  HIV  proteins and cocaine results in the attenuation of antiproliferative bone morphogenetic protein receptor‐2 ( BMPR 2) protein expression without any decrease in its  mRNA  levels. Therefore, in this study, we aimed to investigate the micro  RNA ‐mediated posttranscriptional regulation of  BMPR 2 expression.    Methods and Results  We identified a network of  BMPR 2 targeting micro  RNA s including miR‐216a to be upregulated in response to cocaine and Tat‐mediated augmentation of oxidative stress and transforming growth factor‐β signaling in human pulmonary arterial smooth muscle cells. By using a loss or gain of function studies, we observed that these upregulated micro  RNA s are involved in the Tat‐ and cocaine‐mediated smooth muscle hyperplasia via regulation of  BMPR 2 protein expression. These in vitro findings were further corroborated using rat pulmonary arterial smooth muscle cells isolated from  HIV  transgenic rats exposed to cocaine. More importantly, luciferase reporter and in vitro translation assays demonstrated that direct binding of novel miR‐216a and miR‐301a to 3′ UTR  of  BMPR 2 results in the translational repression of  BMPR 2 without any degradation of its  mRNA .    Conclusions  We identified for the first time miR‐216a as a negative modulator of  BMPR 2 translation and observed it to be involved in  HIV  protein(s) and cocaine‐mediated enhanced proliferation of pulmonary smooth muscle cells.

journal of the american heart association

Network of Micro RNA s Mediate Translational Repression of Bone Morphogenetic Protein Receptor‐2: Involvement in  HIV ‐Associated Pulmonary Vascular Remodeling