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10.1152/ajplung.00350.2015 http://scihub22266oqcxt.onion/10.1152/ajplung.00350.2015 C4867351!4867351!26944089     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 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 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 276.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 276.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 276.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 276.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Physiol+Lung+Cell+Mol+Physiol 2016 ; 310 (9): L824-36 Nephropedia Template TP {{tp|p=26944089|t=2016. ?-Smooth muscle actin is an inconsistent marker of fibroblasts responsible for force-dependent TGF? activation or collagen production across multiple models of organ fibrosis |pdf=|usr=}}{{26944089}} gab.com Text -Smooth muscle actin is an inconsistent marker of fibroblasts responsible for force-dependent TGF activation or collagen production across multiple models of organ fibrosis JO: Am J Physiol Lung Cell Mol Physiol http://www.kidney.de/pget.php?&tw=1&pmid=26944089 #FOAvip Fibrosis is a common pathological sequela of tissue injury or inflammation, and is a major cause of organ failure. Subsets of fibroblasts contribute to tissue fibrosis in multiple ways, including generating contractile force to activate integrin-bound, latent TGF? and secreting excess amounts of collagens and other extracellular matrix proteins (ECM) that make up pathologic scar. However, the precise fibroblast subsets that drive fibrosis have been poorly understood. In the absence of well-characterized markers, ?-smooth muscle actin (?SMA) is often used to identify pathologic fibroblasts, and some authors have equated ?SMA+ cells with contractile myofibroblasts and proposed that these cells are the major source of ECM. Here, we investigated how well ?SMA expression describes fibroblast subsets responsible for TGF? activation and collagen production in three commonly used models of organ fibrosis that we previously reported could be inhibited by loss of ?v integrins on all fibroblasts (using PDGFR?-Cre). Interestingly, ?SMA-directed deletion of ?v integrins protected mice from CCl4-induced hepatic fibrosis, but not bleomycin-induced pulmonary or unilateral ureteral obstruction?induced renal fibrosis. Using Col-EGFP/?SMA-RFP dual reporter mice, we found that only a minority of collagen-producing cells coexpress ?SMA in the fibrotic lung and kidney. Notably, Col-EGFP+?SMA-RFP? cells isolated from the fibrotic lung and kidney were equally capable of activating TGF? as were Col-EGFP+?SMA-RFP+ cells from the same organ, and this TGF? activation was blocked by a TGF?-blocking antibody and an inhibitor of nonmuscle myosin, respectively. Taken together, our results suggest that ?SMA is an inconsistent marker of contractile and collagen-producing fibroblasts in murine experimental models of organ fibrosis. Twit Text FOAVip -Smooth muscle actin is an inconsistent marker of fibroblasts responsible for force-dependent TGF activation or collagen production across multiple models of organ fibrosis ????Am J Physiol Lung Cell Mol Physiol http://www.kidney.de/pget.php?&tw=1&pmid=26944089 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26944089 #FOAvip English Wikipedia <ref>{{Cite pmid|26944089}}</ref> ?-Smooth muscle actin is an inconsistent marker of fibroblasts responsible for force-dependent TGF? activation or collagen production across multiple models of organ fibrosis #MMPMID26944089 Sun KH; Chang Y; Reed NI; Sheppard D Am J Physiol Lung Cell Mol Physiol 2016[May]; 310 (9): L824-36 PMID26944089show ga Fibrosis is a common pathological sequela of tissue injury or inflammation, and is a major cause of organ failure. Subsets of fibroblasts contribute to tissue fibrosis in multiple ways, including generating contractile force to activate integrin-bound, latent TGF? and secreting excess amounts of collagens and other extracellular matrix proteins (ECM) that make up pathologic scar. However, the precise fibroblast subsets that drive fibrosis have been poorly understood. In the absence of well-characterized markers, ?-smooth muscle actin (?SMA) is often used to identify pathologic fibroblasts, and some authors have equated ?SMA+ cells with contractile myofibroblasts and proposed that these cells are the major source of ECM. Here, we investigated how well ?SMA expression describes fibroblast subsets responsible for TGF? activation and collagen production in three commonly used models of organ fibrosis that we previously reported could be inhibited by loss of ?v integrins on all fibroblasts (using PDGFR?-Cre). Interestingly, ?SMA-directed deletion of ?v integrins protected mice from CCl4-induced hepatic fibrosis, but not bleomycin-induced pulmonary or unilateral ureteral obstruction?induced renal fibrosis. Using Col-EGFP/?SMA-RFP dual reporter mice, we found that only a minority of collagen-producing cells coexpress ?SMA in the fibrotic lung and kidney. Notably, Col-EGFP+?SMA-RFP? cells isolated from the fibrotic lung and kidney were equally capable of activating TGF? as were Col-EGFP+?SMA-RFP+ cells from the same organ, and this TGF? activation was blocked by a TGF?-blocking antibody and an inhibitor of nonmuscle myosin, respectively. Taken together, our results suggest that ?SMA is an inconsistent marker of contractile and collagen-producing fibroblasts in murine experimental models of organ fibrosis. ä?-Smooth muscle actin is an inconsistent marker of fibroblasts respons(epmc).pdf DeepDyve Pubget Overpricing