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10.2147/IJNRD.S141393 http://scihub22266oqcxt.onion/10.2147/IJNRD.S141393 C5587152!5587152!28919801     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28919801&cmd=llinks): Failed to open stream: HTTP request failed! 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Transforming growth factor-?1/Smad3-independent epithelial?mesenchymal transition in type I collagen glomerulopathy |pdf=|usr=}}{{28919801}} gab.com Text Transforming growth factor- 1/Smad3-independent epithelial mesenchymal transition in type I collagen glomerulopathy JO: Int J Nephrol Renovasc Dis http://www.kidney.de/pget.php?&tw=1&pmid=28919801 #FOAvip The glomerulofibrotic Col1a2-deficient mouse model demonstrates glomerular homotrimeric type I collagen deposition in mesangial and subendothelial spaces. In this report, we investigate the role of transforming growth factor ?1 (TGF-?1) in myofibroblast activation and epithelial?mesenchymal transition (EMT) in this glomerulopathy. Immunohistochemical analyses of glomerular ?-sma, desmin, vimentin, and proliferating cell nuclear antigen demonstrated parietal epithelial cell proliferation and EMT in late stages of the glomerulopathy in the Col1a2-deficient mice. Glomerular TGF-?1 RNA and protein were not elevated in 1- and 3-month-old mice as determined by quantitative reverse transcriptase-polymerase chain reaction and protein immunoassay analyses. To investigate further whether TGF-?1 plays a role in the glomerulopathy outside of the 1- and 3-month time periods, the Col1a2-deficient mice were bred with Smad3 knockout mice. If the glomerular fibrosis in the Col1a2-deficient mice is mediated by the TGF-?1/Smad3 transcription pathway, it was hypothesized that the resultant Col1a2-deficient/Smad3-deficient mice would exhibit attenuated glomerular homotrimer deposition. However, the Col1a2-deficient/Smad3-deficient kidneys were similarly affected as compared to age-matched Col1a2-deficient kidneys, suggesting that homotrimeric type I collagen deposition in the Col1a2-deficient mouse is independent of TGF-?1/Smad3 signaling. Deposition of homotrimeric type I collagen appears to be the initiating event in this glomerulopathy, providing evidence that EMT and myofibroblast activation occur following initiation, consistent with a secondary wound-healing response independent of TGF-?1. Twit Text FOAVip Transforming growth factor- 1/Smad3-independent epithelial mesenchymal transition in type I collagen glomerulopathy ????Int J Nephrol Renovasc Dis http://www.kidney.de/pget.php?&tw=1&pmid=28919801 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28919801 #FOAvip English Wikipedia <ref>{{Cite pmid|28919801}}</ref> Transforming growth factor-?1/Smad3-independent epithelial?mesenchymal transition in type I collagen glomerulopathy #MMPMID28919801 Brodeur AC; Roberts-Pilgrim AM; Thompson KL; Franklin CL; Phillips CL Int J Nephrol Renovasc Dis 2017[]; 10 (ä): 251-9 PMID28919801show ga The glomerulofibrotic Col1a2-deficient mouse model demonstrates glomerular homotrimeric type I collagen deposition in mesangial and subendothelial spaces. In this report, we investigate the role of transforming growth factor ?1 (TGF-?1) in myofibroblast activation and epithelial?mesenchymal transition (EMT) in this glomerulopathy. Immunohistochemical analyses of glomerular ?-sma, desmin, vimentin, and proliferating cell nuclear antigen demonstrated parietal epithelial cell proliferation and EMT in late stages of the glomerulopathy in the Col1a2-deficient mice. Glomerular TGF-?1 RNA and protein were not elevated in 1- and 3-month-old mice as determined by quantitative reverse transcriptase-polymerase chain reaction and protein immunoassay analyses. To investigate further whether TGF-?1 plays a role in the glomerulopathy outside of the 1- and 3-month time periods, the Col1a2-deficient mice were bred with Smad3 knockout mice. If the glomerular fibrosis in the Col1a2-deficient mice is mediated by the TGF-?1/Smad3 transcription pathway, it was hypothesized that the resultant Col1a2-deficient/Smad3-deficient mice would exhibit attenuated glomerular homotrimer deposition. However, the Col1a2-deficient/Smad3-deficient kidneys were similarly affected as compared to age-matched Col1a2-deficient kidneys, suggesting that homotrimeric type I collagen deposition in the Col1a2-deficient mouse is independent of TGF-?1/Smad3 signaling. Deposition of homotrimeric type I collagen appears to be the initiating event in this glomerulopathy, providing evidence that EMT and myofibroblast activation occur following initiation, consistent with a secondary wound-healing response independent of TGF-?1. äTransforming growth factor-?1/Smad3-independent epithelial?mesenchymal(epmc).pdf DeepDyve Pubget Overpricing