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10.1513/AnnalsATS.201406-245MG http://scihub22266oqcxt.onion/10.1513/AnnalsATS.201406-245MG C4430968!4430968 !25830829     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25830829 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Ann+Am+Thorac+Soc 2015 ; 12 Suppl 1 (Suppl 1 ): S21-3 Nephropedia Template TP {{tp|p=25830829 |t=2015. Epithelial-mesenchymal interactions in fibrosis and repair Transforming growth factor-? activation by epithelial cells and fibroblasts |pdf=|usr=}}{{25830829 }} gab.com Text Epithelial-mesenchymal interactions in fibrosis and repair Transforming growth factor- activation by epithelial cells and fibroblasts JO: Ann Am Thorac Soc http://www.kidney.de/pget.php?&tw=1&pmid=25830829 #FOAvip Transforming growth factor-? (TGF-?) plays a central role in driving tissue fibrosis. TGF-? is secreted in a latent form, held latent by noncovalent association of the active cytokine with a peptide derived from cleavage of the N-terminal domain of the same gene product, and needs to be activated extracellularly to exert any of its diverse biological effects. We have shown that two of the three mammalian isoforms of TGF-?, TGF-?1 and TGF-?3, depend on interactions with cell surface integrins for activation. We found that the integrin ?v?6 is highly induced on injured alveolar epithelial cells, potently induces TGF-? activation, and is critical for the development of pulmonary fibrosis and acute lung injury. However, although TGF-? drives fibrosis in virtually every anatomic site, ?v?6-mediated TGF-? activation is much more restricted. For example, ?v?6 is not induced on injured hepatocytes and plays little or no role in cirrhosis induced by repetitive hepatocyte injury. Fibroblasts are highly contractile cells that express multiple integrins closely related to ?v?6, which share the promiscuous ?v subunit, so we reasoned that perhaps one or more of these ?v integrins on fibroblasts might substitute for ?v?6 and activate the TGF-? required to drive liver fibrosis. Indeed, deletion of the ?v subunit from activated fibroblasts protected mice from carbon tetrachloride-induced liver fibrosis. Importantly, these same mice were protected from bleomycin-induced pulmonary fibrosis and renal fibrosis caused by unilateral ureteral obstruction, despite the presence of epithelial ?v?6 in these mice. These results suggest that the generation and maintenance of sufficient quantities of active TGF-? to cause tissue fibrosis in multiple organs probably depends on at least two sources-TGF-? activation by injured epithelial cells that drives fibroblast expansion and activation and an amplification step that involves TGF-? activation by an ?v integrin on activated fibroblasts. These results suggest that intervening at either of these steps could be useful for the treatment of fibrotic diseases. Twit Text FOAVip Epithelial-mesenchymal interactions in fibrosis and repair Transforming growth factor- activation by epithelial cells and fibroblasts ????Ann Am Thorac Soc http://www.kidney.de/pget.php?&tw=1&pmid=25830829 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25830829 #FOAvip English Wikipedia <ref>{{Cite pmid|25830829 }}</ref> Epithelial-mesenchymal interactions in fibrosis and repair Transforming growth factor-? activation by epithelial cells and fibroblasts #MMPMID25830829 Sheppard D Ann Am Thorac Soc 2015[Mar]; 12 Suppl 1 (Suppl 1 ): S21-3 PMID25830829 show ga Transforming growth factor-? (TGF-?) plays a central role in driving tissue fibrosis. TGF-? is secreted in a latent form, held latent by noncovalent association of the active cytokine with a peptide derived from cleavage of the N-terminal domain of the same gene product, and needs to be activated extracellularly to exert any of its diverse biological effects. We have shown that two of the three mammalian isoforms of TGF-?, TGF-?1 and TGF-?3, depend on interactions with cell surface integrins for activation. We found that the integrin ?v?6 is highly induced on injured alveolar epithelial cells, potently induces TGF-? activation, and is critical for the development of pulmonary fibrosis and acute lung injury. However, although TGF-? drives fibrosis in virtually every anatomic site, ?v?6-mediated TGF-? activation is much more restricted. For example, ?v?6 is not induced on injured hepatocytes and plays little or no role in cirrhosis induced by repetitive hepatocyte injury. Fibroblasts are highly contractile cells that express multiple integrins closely related to ?v?6, which share the promiscuous ?v subunit, so we reasoned that perhaps one or more of these ?v integrins on fibroblasts might substitute for ?v?6 and activate the TGF-? required to drive liver fibrosis. Indeed, deletion of the ?v subunit from activated fibroblasts protected mice from carbon tetrachloride-induced liver fibrosis. Importantly, these same mice were protected from bleomycin-induced pulmonary fibrosis and renal fibrosis caused by unilateral ureteral obstruction, despite the presence of epithelial ?v?6 in these mice. These results suggest that the generation and maintenance of sufficient quantities of active TGF-? to cause tissue fibrosis in multiple organs probably depends on at least two sources-TGF-? activation by injured epithelial cells that drives fibroblast expansion and activation and an amplification step that involves TGF-? activation by an ?v integrin on activated fibroblasts. These results suggest that intervening at either of these steps could be useful for the treatment of fibrotic diseases. |Animals [MESH] |Antigens, Neoplasm/metabolism [MESH] |Epithelial Cells/*metabolism [MESH] |Fibroblasts/*metabolism [MESH] |Humans [MESH] |Integrins/metabolism [MESH] |Liver Cirrhosis/*metabolism/therapy [MESH] |Mice [MESH] |Pulmonary Fibrosis/*metabolism/therapy [MESH]Epithelial-mesenchymal interactions in fibrosis and repair Transformi(epmc).pdf DeepDyve Pubget Overpricing