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10.1038/boneres.2017.8 http://scihub22266oqcxt.onion/10.1038/boneres.2017.8 C5360159!5360159 !28392965     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28392965 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Bone+Res 2017 ; 5 (?): 17008 Nephropedia Template TP {{tp|p=28392965 |t=2017. Mechanosignaling activation of TGF? maintains intervertebral disc homeostasis |pdf=|usr=}}{{28392965 }} gab.com Text Mechanosignaling activation of TGF maintains intervertebral disc homeostasis JO: Bone Res http://www.kidney.de/pget.php?&tw=1&pmid=28392965 #FOAvip Intervertebral disc (IVD) degeneration is the leading cause of disability with no disease-modifying treatment. IVD degeneration is associated with instable mechanical loading in the spine, but little is known about how mechanical stress regulates nucleus notochordal (NC) cells to maintain IVD homeostasis. Here we report that mechanical stress can result in excessive integrin ?(v)?(6)-mediated activation of transforming growth factor beta (TGF?), decreased NC cell vacuoles, and increased matrix proteoglycan production, and results in degenerative disc disease (DDD). Knockout of TGF? type II receptor (T?RII) or integrin ?(v) in the NC cells inhibited functional activity of postnatal NC cells and also resulted in DDD under mechanical loading. Administration of RGD peptide, TGF?, and ?(v)?(6)-neutralizing antibodies attenuated IVD degeneration. Thus, integrin-mediated activation of TGF? plays a critical role in mechanical signaling transduction to regulate IVD cell function and homeostasis. Manipulation of this signaling pathway may be a potential therapeutic target to modify DDD. Twit Text FOAVip Mechanosignaling activation of TGF maintains intervertebral disc homeostasis ????Bone Res http://www.kidney.de/pget.php?&tw=1&pmid=28392965 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28392965 #FOAvip English Wikipedia <ref>{{Cite pmid|28392965 }}</ref> Mechanosignaling activation of TGF? maintains intervertebral disc homeostasis #MMPMID28392965 Bian Q ; Ma L ; Jain A ; Crane JL ; Kebaish K ; Wan M ; Zhang Z ; Edward Guo X ; Sponseller PD ; Séguin CA ; Riley LH ; Wang Y ; Cao X Bone Res 2017[]; 5 (?): 17008 PMID28392965 show ga Intervertebral disc (IVD) degeneration is the leading cause of disability with no disease-modifying treatment. IVD degeneration is associated with instable mechanical loading in the spine, but little is known about how mechanical stress regulates nucleus notochordal (NC) cells to maintain IVD homeostasis. Here we report that mechanical stress can result in excessive integrin ?(v)?(6)-mediated activation of transforming growth factor beta (TGF?), decreased NC cell vacuoles, and increased matrix proteoglycan production, and results in degenerative disc disease (DDD). Knockout of TGF? type II receptor (T?RII) or integrin ?(v) in the NC cells inhibited functional activity of postnatal NC cells and also resulted in DDD under mechanical loading. Administration of RGD peptide, TGF?, and ?(v)?(6)-neutralizing antibodies attenuated IVD degeneration. Thus, integrin-mediated activation of TGF? plays a critical role in mechanical signaling transduction to regulate IVD cell function and homeostasis. Manipulation of this signaling pathway may be a potential therapeutic target to modify DDD. ?Mechanosignaling activation of TGF? maintains intervertebral disc home(epmc).pdf DeepDyve Pubget Overpricing