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10.1038/srep22729 http://scihub22266oqcxt.onion/10.1038/srep22729 C4778133!4778133 !26940839     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26940839 &cmd=llinks): Failed to open stream: HTTP request failed! 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MiR-630 Inhibits Endothelial-Mesenchymal Transition by Targeting Slug in Traumatic Heterotopic Ossification |pdf=|usr=}}{{26940839 }} gab.com Text MiR-630 Inhibits Endothelial-Mesenchymal Transition by Targeting Slug in Traumatic Heterotopic Ossification JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26940839 #FOAvip Heterotopic ossification (HO) is the abnormal formation of mature bone in extraskeletal soft tissues that occurs as a result of inflammation caused by traumatic injury or associated with genetic mutation. Despite extensive research to identify the source of osteogenic progenitors, the cellular origins of HO are controversial and the underlying mechanisms, which are important for the early detection of HO, remain unclear. Here, we used in vitro and in vivo models of BMP4 and TGF-?2-induced HO to identify the cellular origin and the mechanisms mediating the formation of ectopic bone in traumatic HO. Our results suggest an endothelial origin of ectopic bone in early phase of traumatic HO and indicate that the inhibition of endothelial-mesenchymal transition by miR-630 targeting Slug plays a role in the formation of ectopic bone in HO. A matched case-control study showed that miR-630 is specifically downregulated during the early stages of HO and can be used to distinguish HO from other processes leading to bone formation. Our findings suggest a potential mechanism of post-traumatic ectopic bone formation and identify miR-630 as a potential early indicator of HO. Twit Text FOAVip MiR-630 Inhibits Endothelial-Mesenchymal Transition by Targeting Slug in Traumatic Heterotopic Ossification ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26940839 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26940839 #FOAvip English Wikipedia <ref>{{Cite pmid|26940839 }}</ref> MiR-630 Inhibits Endothelial-Mesenchymal Transition by Targeting Slug in Traumatic Heterotopic Ossification #MMPMID26940839 Sun Y ; Cai J ; Yu S ; Chen S ; Li F ; Fan C Sci Rep 2016[Mar]; 6 (ä): 22729 PMID26940839 show ga Heterotopic ossification (HO) is the abnormal formation of mature bone in extraskeletal soft tissues that occurs as a result of inflammation caused by traumatic injury or associated with genetic mutation. Despite extensive research to identify the source of osteogenic progenitors, the cellular origins of HO are controversial and the underlying mechanisms, which are important for the early detection of HO, remain unclear. Here, we used in vitro and in vivo models of BMP4 and TGF-?2-induced HO to identify the cellular origin and the mechanisms mediating the formation of ectopic bone in traumatic HO. Our results suggest an endothelial origin of ectopic bone in early phase of traumatic HO and indicate that the inhibition of endothelial-mesenchymal transition by miR-630 targeting Slug plays a role in the formation of ectopic bone in HO. A matched case-control study showed that miR-630 is specifically downregulated during the early stages of HO and can be used to distinguish HO from other processes leading to bone formation. Our findings suggest a potential mechanism of post-traumatic ectopic bone formation and identify miR-630 as a potential early indicator of HO. |*Gene Expression Regulation [MESH] |*Ossification, Heterotopic [MESH] |Adolescent [MESH] |Adult [MESH] |Animals [MESH] |Case-Control Studies [MESH] |Child [MESH] |Endothelium/*physiology [MESH] |Female [MESH] |Humans [MESH] |Male [MESH] |Mesoderm/*physiology [MESH] |Mice, Inbred BALB C [MESH] |MicroRNAs/*metabolism [MESH] |Middle Aged [MESH] |Snail Family Transcription Factors/*metabolism [MESH] |Wounds and Injuries/*complications [MESH]MiR-630 Inhibits Endothelial-Mesenchymal Transition by Targeting Slug (epmc).pdf DeepDyve Pubget Overpricing