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10.1371/journal.pone.0184388 http://scihub22266oqcxt.onion/10.1371/journal.pone.0184388 C5604944!5604944!28926590     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+One 2017 ; 12 (9): ä Nephropedia Template TP {{tp|p=28926590|t=2017. Fluoxetine ameliorates cartilage degradation in osteoarthritis by inhibiting Wnt/?-catenin signaling |pdf=|usr=}}{{28926590}} gab.com Text Fluoxetine ameliorates cartilage degradation in osteoarthritis by inhibiting Wnt/ -catenin signaling JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=28926590 #FOAvip Abnormal activation of the Wnt/?-catenin signaling is implicated in the osteoarthritis (OA) pathology. We searched for a pre-approved drug that suppresses abnormally activated Wnt/?-catenin signaling and has a potency to reduce joint pathology in OA. We introduced the TOPFlash reporter plasmid into HCS-2/8 human chondrosarcoma cells to estimate the Wnt/?-catenin activity in the presence of 10 ?M each compound in a panel of pre-approved drugs. We found that fluoxetine, an antidepressant in the class of selective serotonin reuptake inhibitors (SSRI), down-regulated Wnt/?-catenin signaling in human chondrosarcoma cells. Fluoxetine inhibited both Wnt3A- and LiCl-induced loss of proteoglycans in chondrogenically differentiated ATDC5 cells. Fluoxetine increased expression of Sox9 (the chondrogenic master regulator), and decreased expressions of Axin2 (a marker for Wnt/?-catenin signaling) and Mmp13 (matrix metalloproteinase 13). Fluoxetine suppressed a LiCl-induced increase of total ?-catenin and a LiCl-induced decrease of phosphorylated ?-catenin in a dose-dependent manner. An in vitro protein-binding assay showed that fluoxetine enhanced binding of ?-catenin with Axin1, which is a scaffold protein forming the degradation complex for ?-catenin. Fluoxetine suppressed LiCl-induced ?-catenin accumulation in human OA chondrocytes. Intraarticular injection of fluoxetine in a rat OA model ameliorated OA progression and suppressed ?-catenin accumulation. Twit Text FOAVip Fluoxetine ameliorates cartilage degradation in osteoarthritis by inhibiting Wnt/ -catenin signaling ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=28926590 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28926590 #FOAvip English Wikipedia <ref>{{Cite pmid|28926590}}</ref> Fluoxetine ameliorates cartilage degradation in osteoarthritis by inhibiting Wnt/?-catenin signaling #MMPMID28926590 Miyamoto K; Ohkawara B; Ito M; Masuda A; Hirakawa A; Sakai T; Hiraiwa H; Hamada T; Ishiguro N; Ohno K PLoS One 2017[]; 12 (9): ä PMID28926590show ga Abnormal activation of the Wnt/?-catenin signaling is implicated in the osteoarthritis (OA) pathology. We searched for a pre-approved drug that suppresses abnormally activated Wnt/?-catenin signaling and has a potency to reduce joint pathology in OA. We introduced the TOPFlash reporter plasmid into HCS-2/8 human chondrosarcoma cells to estimate the Wnt/?-catenin activity in the presence of 10 ?M each compound in a panel of pre-approved drugs. We found that fluoxetine, an antidepressant in the class of selective serotonin reuptake inhibitors (SSRI), down-regulated Wnt/?-catenin signaling in human chondrosarcoma cells. Fluoxetine inhibited both Wnt3A- and LiCl-induced loss of proteoglycans in chondrogenically differentiated ATDC5 cells. Fluoxetine increased expression of Sox9 (the chondrogenic master regulator), and decreased expressions of Axin2 (a marker for Wnt/?-catenin signaling) and Mmp13 (matrix metalloproteinase 13). Fluoxetine suppressed a LiCl-induced increase of total ?-catenin and a LiCl-induced decrease of phosphorylated ?-catenin in a dose-dependent manner. An in vitro protein-binding assay showed that fluoxetine enhanced binding of ?-catenin with Axin1, which is a scaffold protein forming the degradation complex for ?-catenin. Fluoxetine suppressed LiCl-induced ?-catenin accumulation in human OA chondrocytes. Intraarticular injection of fluoxetine in a rat OA model ameliorated OA progression and suppressed ?-catenin accumulation. äFluoxetine ameliorates cartilage degradation in osteoarthritis by inhi(epmc).pdf DeepDyve Pubget Overpricing