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10.1016/j.exer.2016.04.007 http://scihub22266oqcxt.onion/10.1016/j.exer.2016.04.007 C5310225!5310225!27091054     free     free     free Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Exp+Eye+Res 2016 ; 148 (ä): 97-102 Nephropedia Template TP {{tp|p=27091054|t=2016. Crosstalk between TGF? and Wnt Signaling Pathways in the Human Trabecular Meshwork |pdf=|usr=}}{{27091054}} gab.com Text Crosstalk between TGF and Wnt Signaling Pathways in the Human Trabecular Meshwork JO: Exp Eye Res http://www.kidney.de/pget.php?&tw=1&pmid=27091054 #FOAvip Primary Open Angle Glaucoma (POAG) is an irreversible, vision-threatening disease that affects millions worldwide. The principal risk factor of POAG is increased intraocular pressure (IOP) due to pathological changes in the trabecular meshwork (TM). The TGF? signaling pathway activator TGF?2 and the Wnt signaling pathway inhibitor secreted frizzled-related protein 1 (SFRP1) are elevated in the POAG TM. In this study, we determined whether there is a crosstalk between the TGF?/Smad pathway and the canonical Wnt pathway using luciferase reporter assays. Lentiviral luciferase reporter vectors for studying the TGF?/Smad pathway or the canonical Wnt pathway were transduced into primary human non-glaucomatous TM (NTM) cells. Cells were treated with or without a combination of 5?g/ml TGF?2 and/or 100ng/ml Wnt3a recombinant proteins, and luciferase levels were measured using a plate reader. We found that TGF?2 inhibited Wnt3a-induced canonical Wnt pathway activation, while Wnt3a inhibited TGF?2-induced TGF?/Smad pathway activation (n=6, p<0.05) in 3 NTM cell strains. We also found that knocking down of Smad4 or ?-catenin using siRNA in HTM5 cells transfected with similar luciferase reporter plasmids abolished the inhibitory effect of TGF?2 and/or Wnt3a on the other pathway (n=6). Our results suggest the existence of a cross-inhibition between the TGF?/Smad and canonical Wnt pathways in the TM, and this cross-inhibition may be mediated by Smad4 and ?-catenin. Twit Text FOAVip Crosstalk between TGF and Wnt Signaling Pathways in the Human Trabecular Meshwork ????Exp Eye Res http://www.kidney.de/pget.php?&tw=1&pmid=27091054 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27091054 #FOAvip English Wikipedia <ref>{{Cite pmid|27091054}}</ref> Crosstalk between TGF? and Wnt Signaling Pathways in the Human Trabecular Meshwork #MMPMID27091054 Webber HC; Bermudez JY; Sethi A; Clark AF; Mao W Exp Eye Res 2016[Jul]; 148 (ä): 97-102 PMID27091054show ga Primary Open Angle Glaucoma (POAG) is an irreversible, vision-threatening disease that affects millions worldwide. The principal risk factor of POAG is increased intraocular pressure (IOP) due to pathological changes in the trabecular meshwork (TM). The TGF? signaling pathway activator TGF?2 and the Wnt signaling pathway inhibitor secreted frizzled-related protein 1 (SFRP1) are elevated in the POAG TM. In this study, we determined whether there is a crosstalk between the TGF?/Smad pathway and the canonical Wnt pathway using luciferase reporter assays. Lentiviral luciferase reporter vectors for studying the TGF?/Smad pathway or the canonical Wnt pathway were transduced into primary human non-glaucomatous TM (NTM) cells. Cells were treated with or without a combination of 5?g/ml TGF?2 and/or 100ng/ml Wnt3a recombinant proteins, and luciferase levels were measured using a plate reader. We found that TGF?2 inhibited Wnt3a-induced canonical Wnt pathway activation, while Wnt3a inhibited TGF?2-induced TGF?/Smad pathway activation (n=6, p<0.05) in 3 NTM cell strains. We also found that knocking down of Smad4 or ?-catenin using siRNA in HTM5 cells transfected with similar luciferase reporter plasmids abolished the inhibitory effect of TGF?2 and/or Wnt3a on the other pathway (n=6). Our results suggest the existence of a cross-inhibition between the TGF?/Smad and canonical Wnt pathways in the TM, and this cross-inhibition may be mediated by Smad4 and ?-catenin. äCrosstalk between TGF? and Wnt Signaling Pathways in the Human Trabecu(epmc).pdf DeepDyve Pubget Overpricing