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10.1096/fj.201600428R http://scihub22266oqcxt.onion/10.1096/fj.201600428R C5067255!5067255 !27480571     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27480571 &cmd=llinks): Failed to open stream: HTTP request failed! 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Profibrotic up-regulation of glucose transporter 1 by TGF-? involves activation of MEK and mammalian target of rapamycin complex 2 pathways |pdf=|usr=}}{{27480571 }} gab.com Text Profibrotic up-regulation of glucose transporter 1 by TGF- involves activation of MEK and mammalian target of rapamycin complex 2 pathways JO: FASEB J http://www.kidney.de/pget.php?&tw=1&pmid=27480571 #FOAvip TGF-? plays a central role in the pathogenesis of fibroproliferative disorders. Defining the exact underlying molecular basis is therefore critical for the development of viable therapeutic strategies. Here, we show that expression of the facilitative glucose transporter 1 (GLUT1) is induced by TGF-? in fibroblast lines and primary cells and is required for the profibrotic effects of TGF-?. In addition, enhanced GLUT1 expression is observed in fibrotic areas of lungs of both patients with idiopathic pulmonary fibrosis and mice that are subjected to a fibrosis-inducing bleomycin treatment. By using pharmacologic and genetic approaches, we demonstrate that up-regulation of GLUT1 occurs via the canonical Smad2/3 pathway and requires autocrine activation of the receptor tyrosine kinases, platelet-derived and epidermal growth factor receptors. Engagement of the common downstream effector PI3K subsequently triggers activation of the MEK and mammalian target of rapamycin complex 2, which cooperate in regulating GLUT1 expression. Of note, inhibition of GLUT1 activity and/or expression is shown to impair TGF-?-driven fibrogenic processes, including cell proliferation and production of profibrotic mediators. These findings provide new perspectives on the interrelation of metabolism and profibrotic TGF-? signaling and present opportunities for potential therapeutic intervention.-Andrianifahanana, M., Hernandez, D. M., Yin, X., Kang, J.-H., Jung, M.-Y., Wang, Y., Yi, E. S., Roden, A. C., Limper, A. H., Leof, E. B. Profibrotic up-regulation of glucose transporter 1 by TGF-? involves activation of MEK and mammalian target of rapamycin complex 2 pathways. Twit Text FOAVip Profibrotic up-regulation of glucose transporter 1 by TGF- involves activation of MEK and mammalian target of rapamycin complex 2 pathways ????FASEB J http://www.kidney.de/pget.php?&tw=1&pmid=27480571 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27480571 #FOAvip English Wikipedia <ref>{{Cite pmid|27480571 }}</ref> Profibrotic up-regulation of glucose transporter 1 by TGF-? involves activation of MEK and mammalian target of rapamycin complex 2 pathways #MMPMID27480571 Andrianifahanana M ; Hernandez DM ; Yin X ; Kang JH ; Jung MY ; Wang Y ; Yi ES ; Roden AC ; Limper AH ; Leof EB FASEB J 2016[Nov]; 30 (11 ): 3733-3744 PMID27480571 show ga TGF-? plays a central role in the pathogenesis of fibroproliferative disorders. Defining the exact underlying molecular basis is therefore critical for the development of viable therapeutic strategies. Here, we show that expression of the facilitative glucose transporter 1 (GLUT1) is induced by TGF-? in fibroblast lines and primary cells and is required for the profibrotic effects of TGF-?. In addition, enhanced GLUT1 expression is observed in fibrotic areas of lungs of both patients with idiopathic pulmonary fibrosis and mice that are subjected to a fibrosis-inducing bleomycin treatment. By using pharmacologic and genetic approaches, we demonstrate that up-regulation of GLUT1 occurs via the canonical Smad2/3 pathway and requires autocrine activation of the receptor tyrosine kinases, platelet-derived and epidermal growth factor receptors. Engagement of the common downstream effector PI3K subsequently triggers activation of the MEK and mammalian target of rapamycin complex 2, which cooperate in regulating GLUT1 expression. Of note, inhibition of GLUT1 activity and/or expression is shown to impair TGF-?-driven fibrogenic processes, including cell proliferation and production of profibrotic mediators. These findings provide new perspectives on the interrelation of metabolism and profibrotic TGF-? signaling and present opportunities for potential therapeutic intervention.-Andrianifahanana, M., Hernandez, D. M., Yin, X., Kang, J.-H., Jung, M.-Y., Wang, Y., Yi, E. S., Roden, A. C., Limper, A. H., Leof, E. B. Profibrotic up-regulation of glucose transporter 1 by TGF-? involves activation of MEK and mammalian target of rapamycin complex 2 pathways. |Animals [MESH] |Cell Proliferation/*physiology [MESH] |Connective Tissue Growth Factor/metabolism [MESH] |Fibroblasts/metabolism [MESH] |Fibrosis/metabolism [MESH] |Glucose Transporter Type 1/*metabolism [MESH] |Lung/metabolism [MESH] |MAP Kinase Signaling System/*physiology [MESH] |Mice [MESH] |Phosphatidylinositol 3-Kinases/metabolism [MESH] |Signal Transduction/physiology [MESH] |Sirolimus/*metabolism [MESH] |Transforming Growth Factor beta/*metabolism [MESH]Profibrotic up-regulation of glucose transporter 1 by TGF-? involves a(epmc).pdf DeepDyve Pubget Overpricing