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10.1074/jbc.M117.783308 http://scihub22266oqcxt.onion/10.1074/jbc.M117.783308 C5448094!5448094 !28377507     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28377507 &cmd=llinks): Failed to open stream: HTTP request failed! 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An epigenetic regulatory loop controls pro-osteogenic activation by TGF-?1 or bone morphogenetic protein 2 in human aortic valve interstitial cells |pdf=|usr=}}{{28377507 }} gab.com Text An epigenetic regulatory loop controls pro-osteogenic activation by TGF- 1 or bone morphogenetic protein 2 in human aortic valve interstitial cells JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=28377507 #FOAvip Calcific aortic valve disease (CAVD) is common in the elderly population, but pharmacological interventions for managing valvular calcification are unavailable. Transforming growth factor ?1 (TGF-?1) and bone morphogenetic protein 2 (BMP-2) induce pro-osteogenic activation of human aortic valve interstitial cells (AVICs) that play an important role in valvular calcification. However, the molecular mechanism underlying pro-osteogenic activation in AVICs is incompletely understood. Here, we investigated an epigenetic regulatory mechanism in human AVIC pro-osteogenic activation induced by TGF-?1 and BMP-2. Microarray and real-time PCR analyses revealed that microRNA (miR)-486 up-regulation and miR-204 down-regulation were characteristic changes in TGF-?1- and BMP-2-stimulated normal AVICs and in AVICs from calcified valves. Both TGF-?1 and BMP-2 down-regulated miR-204 through Smad pathways. Interestingly, an miR-486 antagomir diminished the effect of TGF-?1 and BMP-2 on miR-204 levels and calcium deposit formation. Furthermore, the miR-486 antagomir increased the expression of Smurf2, a Smad inhibitor, in the presence or absence of TGF-?1 or BMP-2 stimulation, whereas a miR-486 mimic reduced Smurf2 expression. Smurf2 knockdown augmented TGF-?1- or BMP-2-induced miR-204 down-regulation and resulted in increased expression of the osteoblastic biomarkers Osx and Runx2. In summary, we found that TGF-?1 and BMP-2 up-regulate miR-486 and down-regulate miR-204 in human AVICs to promote pro-osteogenic activity and that miR-486 inhibits Smurf2 expression to augment the miR-204 down-regulation. We conclude that the miR-486-Smurf2-Smad loop plays an important role in regulating AVIC pro-osteogenic activation in response to TGF-?1 or BMP-2. Targeting this regulatory loop may have therapeutic potential for suppressing aortic valve calcification. Twit Text FOAVip An epigenetic regulatory loop controls pro-osteogenic activation by TGF- 1 or bone morphogenetic protein 2 in human aortic valve interstitial cells ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=28377507 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28377507 #FOAvip English Wikipedia <ref>{{Cite pmid|28377507 }}</ref> An epigenetic regulatory loop controls pro-osteogenic activation by TGF-?1 or bone morphogenetic protein 2 in human aortic valve interstitial cells #MMPMID28377507 Song R ; Fullerton DA ; Ao L ; Zhao KS ; Meng X J Biol Chem 2017[May]; 292 (21 ): 8657-8666 PMID28377507 show ga Calcific aortic valve disease (CAVD) is common in the elderly population, but pharmacological interventions for managing valvular calcification are unavailable. Transforming growth factor ?1 (TGF-?1) and bone morphogenetic protein 2 (BMP-2) induce pro-osteogenic activation of human aortic valve interstitial cells (AVICs) that play an important role in valvular calcification. However, the molecular mechanism underlying pro-osteogenic activation in AVICs is incompletely understood. Here, we investigated an epigenetic regulatory mechanism in human AVIC pro-osteogenic activation induced by TGF-?1 and BMP-2. Microarray and real-time PCR analyses revealed that microRNA (miR)-486 up-regulation and miR-204 down-regulation were characteristic changes in TGF-?1- and BMP-2-stimulated normal AVICs and in AVICs from calcified valves. Both TGF-?1 and BMP-2 down-regulated miR-204 through Smad pathways. Interestingly, an miR-486 antagomir diminished the effect of TGF-?1 and BMP-2 on miR-204 levels and calcium deposit formation. Furthermore, the miR-486 antagomir increased the expression of Smurf2, a Smad inhibitor, in the presence or absence of TGF-?1 or BMP-2 stimulation, whereas a miR-486 mimic reduced Smurf2 expression. Smurf2 knockdown augmented TGF-?1- or BMP-2-induced miR-204 down-regulation and resulted in increased expression of the osteoblastic biomarkers Osx and Runx2. In summary, we found that TGF-?1 and BMP-2 up-regulate miR-486 and down-regulate miR-204 in human AVICs to promote pro-osteogenic activity and that miR-486 inhibits Smurf2 expression to augment the miR-204 down-regulation. We conclude that the miR-486-Smurf2-Smad loop plays an important role in regulating AVIC pro-osteogenic activation in response to TGF-?1 or BMP-2. Targeting this regulatory loop may have therapeutic potential for suppressing aortic valve calcification. |*Epigenesis, Genetic [MESH] |*Osteogenesis [MESH] |*Signal Transduction [MESH] |Aged [MESH] |Aortic Valve/*metabolism/pathology [MESH] |Bone Morphogenetic Protein 2/*metabolism [MESH] |Cells, Cultured [MESH] |Down-Regulation [MESH] |Female [MESH] |Heart Valve Diseases/*metabolism/pathology [MESH] |Humans [MESH] |Male [MESH] |MicroRNAs/biosynthesis [MESH] |Middle Aged [MESH] |Osteoblasts/metabolism/pathology [MESH] |Transforming Growth Factor beta1/*metabolism [MESH] |Ubiquitin-Protein Ligases/metabolism [MESH] |Up-Regulation [MESH]An epigenetic regulatory loop controls pro-osteogenic activation by TG(epmc).pdf DeepDyve Pubget Overpricing