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10.1093/ndt/gfw308 http://scihub22266oqcxt.onion/10.1093/ndt/gfw308 C5427520!5427520!27566305     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 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 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nephrol+Dial+Transplant 2017 ; 32 (5): 781-91 Nephropedia Template TP {{tp|p=27566305|t=2017. Matrix metalloproteinase 9-dependent Notch signaling contributes to kidney fibrosis through peritubular endothelial?mesenchymal transition |pdf=|usr=}}{{27566305}} gab.com Text Matrix metalloproteinase 9-dependent Notch signaling contributes to kidney fibrosis through peritubular endothelial mesenchymal transition JO: Nephrol Dial Transplant http://www.kidney.de/pget.php?&tw=1&pmid=27566305 #FOAvip Background: Endothelial cells are known to contribute to kidney fibrosis via endothelial?mesenchymal transition (EndoMT). Matrix metalloproteinase 9 (MMP-9) is known to be profibrotic. However, whether MMP-9 contributes to kidney fibrosis via EndoMT is unknown.Methods: Primary mouse renal peritubular endothelial cells (MRPECs) were isolated and treated by recombinant human transforming growth factor beta 1 (rhTGF-?1) with or without MMP-9 inhibitor or by recombinant human MMP-9 (rhMMP-9) alone. Kidney fibrosis was induced by unilateral ureteral obstruction (UUO) in MMP-9 knockout (KO) and wide-type (WT) control mice. The effects of MMP-9 on EndoMT of MRPECs and kidney fibrosis were examined.Results: We showed that MRPECs underwent EndoMT after rhTGF-?1 treatment or in UUO kidney as evidenced by decreased expression of endothelial markers, vascular endothelial cadherin (VE-cadherin) and CD31, and increased levels of mesenchymal markers, ?-smooth muscle actin (?-SMA) and vimentin. The expression of fibrosis markers was also up-regulated significantly after rhTGF-?1 treatment in MRPECs. The EndoMT and fibrosis markers were significantly less in rhTGF-?1-treated MMP-9 KO MRPECs, whereas MMP-9 alone was sufficient to induce EndoMT in MRPECs. UUO kidney of MMP-9 KO mice showed significantly less interstitial fibrosis and EndoMT in MRPECs. Notch signaling shown by Notch intracellular domain (NICD) was increased, while Notch-1 was decreased in rhTGF-?1-treated MRPECs of MMP-9 WT but not MMP-9 KO mice. Inhibition of MMP-9 or Notch signaling prevented rhTGF-?1- or rhMMP-9-induced ?-SMA and NICD upregulation in MRPECs. UUO kidney of MMP-9 KO mice had less staining of Notch signaling transcription factor Hey-1 in VE-cadherin-positive MRPECs than WT controls.Conclusions: Our results demonstrate that MMP-9-dependent Notch signaling plays an important role in kidney fibrosis through EndoMT of MRPECs. Twit Text FOAVip Matrix metalloproteinase 9-dependent Notch signaling contributes to kidney fibrosis through peritubular endothelial mesenchymal transition ????Nephrol Dial Transplant http://www.kidney.de/pget.php?&tw=1&pmid=27566305 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27566305 #FOAvip English Wikipedia <ref>{{Cite pmid|27566305}}</ref> Matrix metalloproteinase 9-dependent Notch signaling contributes to kidney fibrosis through peritubular endothelial?mesenchymal transition #MMPMID27566305 Zhao Y; Qiao X; Tan TK; Zhao H; Zhang Y; Liu L; Zhang J; Wang L; Cao Q; Wang Y; Wang Y; Wang YM; Lee VW; Alexander SI; Harris DC; Zheng G Nephrol Dial Transplant 2017[May]; 32 (5): 781-91 PMID27566305show ga Background: Endothelial cells are known to contribute to kidney fibrosis via endothelial?mesenchymal transition (EndoMT). Matrix metalloproteinase 9 (MMP-9) is known to be profibrotic. However, whether MMP-9 contributes to kidney fibrosis via EndoMT is unknown.Methods: Primary mouse renal peritubular endothelial cells (MRPECs) were isolated and treated by recombinant human transforming growth factor beta 1 (rhTGF-?1) with or without MMP-9 inhibitor or by recombinant human MMP-9 (rhMMP-9) alone. Kidney fibrosis was induced by unilateral ureteral obstruction (UUO) in MMP-9 knockout (KO) and wide-type (WT) control mice. The effects of MMP-9 on EndoMT of MRPECs and kidney fibrosis were examined.Results: We showed that MRPECs underwent EndoMT after rhTGF-?1 treatment or in UUO kidney as evidenced by decreased expression of endothelial markers, vascular endothelial cadherin (VE-cadherin) and CD31, and increased levels of mesenchymal markers, ?-smooth muscle actin (?-SMA) and vimentin. The expression of fibrosis markers was also up-regulated significantly after rhTGF-?1 treatment in MRPECs. The EndoMT and fibrosis markers were significantly less in rhTGF-?1-treated MMP-9 KO MRPECs, whereas MMP-9 alone was sufficient to induce EndoMT in MRPECs. UUO kidney of MMP-9 KO mice showed significantly less interstitial fibrosis and EndoMT in MRPECs. Notch signaling shown by Notch intracellular domain (NICD) was increased, while Notch-1 was decreased in rhTGF-?1-treated MRPECs of MMP-9 WT but not MMP-9 KO mice. Inhibition of MMP-9 or Notch signaling prevented rhTGF-?1- or rhMMP-9-induced ?-SMA and NICD upregulation in MRPECs. UUO kidney of MMP-9 KO mice had less staining of Notch signaling transcription factor Hey-1 in VE-cadherin-positive MRPECs than WT controls.Conclusions: Our results demonstrate that MMP-9-dependent Notch signaling plays an important role in kidney fibrosis through EndoMT of MRPECs. äMatrix metalloproteinase 9-dependent Notch signaling contributes to ki(epmc).pdf DeepDyve Pubget Overpricing