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10.1016/j.matbio.2011.05.003 http://scihub22266oqcxt.onion/10.1016/j.matbio.2011.05.003 C4489541!4489541!21641995     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Matrix+Biol 2011 ; 30 (ä): 318-29 Nephropedia Template TP {{tp|p=21641995|t=2011. Caveolin-1 modulates TGF-?1 signaling in cardiac remodeling |pdf=|usr=}}{{21641995}} gab.com Text Caveolin-1 modulates TGF- 1 signaling in cardiac remodeling JO: Matrix Biol http://www.kidney.de/pget.php?&tw=1&pmid=21641995 #FOAvip The cardiac response to myocardial injury includes fibrotic and hypertrophic processes and a key mediator in this response is transforming growth factor-?1 (TGF-?1). Caveolin-1 (cav1), the main structural protein of caveolae, is an inhibitor of the TGF-?1 signaling pathway. To examine the role of cav1 in cardiac repair, cav1 deficient (Cav1?/?) and wild type (WT) mice were subjected to cryoinjury of the left ventricle (LV). At baseline the two groups exhibited no inflammation, similar collagen content, and similar cardiac function. After injury, Cav1?/? animals displayed enhanced TGF-?1 signaling, as reflected by a 3-fold increase in the activation of the Smad2-dependent pathway and more widespread collagen deposition in the heart. Qualitative and quantitative analysis indicated that collagen deposition peaked in the WT LV 14 days after injury, accompanied by increased mRNA abundance for procol1a2 (2-fold) and procol3a1 (3-fold). Collagen deposition was further enhanced in Cav1?/? mice, which was accompanied by reduced expression of matrix metalloproteinases MMP ?8 (3-fold) and ?13 mRNA (2-fold). The levels of expression of inflammatory markers of acute phase were similar between the strains However, macrophage clearance in the damaged region was delayed in Cav1?/? mice. We observed a 4-fold decrease in collagen deposition in Cav1?/? mice injected with a cav1 scaffolding domain peptide (CSD) and a 2-fold decrease in WT mice treated with the CSD. We conclude that cav1 has a direct role in reducing TGF-?1 signaling and as such might be an appropriate target for therapies to influence cardiac remodeling. Twit Text FOAVip Caveolin-1 modulates TGF- 1 signaling in cardiac remodeling ????Matrix Biol http://www.kidney.de/pget.php?&tw=1&pmid=21641995 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=21641995 #FOAvip English Wikipedia <ref>{{Cite pmid|21641995}}</ref> Caveolin-1 modulates TGF-?1 signaling in cardiac remodeling #MMPMID21641995 Miyasato SK; Loeffler J; Shohet R; Zhang J; Lindsey M; Le Saux CJ Matrix Biol 2011[Jun]; 30 (ä): 318-29 PMID21641995show ga The cardiac response to myocardial injury includes fibrotic and hypertrophic processes and a key mediator in this response is transforming growth factor-?1 (TGF-?1). Caveolin-1 (cav1), the main structural protein of caveolae, is an inhibitor of the TGF-?1 signaling pathway. To examine the role of cav1 in cardiac repair, cav1 deficient (Cav1?/?) and wild type (WT) mice were subjected to cryoinjury of the left ventricle (LV). At baseline the two groups exhibited no inflammation, similar collagen content, and similar cardiac function. After injury, Cav1?/? animals displayed enhanced TGF-?1 signaling, as reflected by a 3-fold increase in the activation of the Smad2-dependent pathway and more widespread collagen deposition in the heart. Qualitative and quantitative analysis indicated that collagen deposition peaked in the WT LV 14 days after injury, accompanied by increased mRNA abundance for procol1a2 (2-fold) and procol3a1 (3-fold). Collagen deposition was further enhanced in Cav1?/? mice, which was accompanied by reduced expression of matrix metalloproteinases MMP ?8 (3-fold) and ?13 mRNA (2-fold). The levels of expression of inflammatory markers of acute phase were similar between the strains However, macrophage clearance in the damaged region was delayed in Cav1?/? mice. We observed a 4-fold decrease in collagen deposition in Cav1?/? mice injected with a cav1 scaffolding domain peptide (CSD) and a 2-fold decrease in WT mice treated with the CSD. We conclude that cav1 has a direct role in reducing TGF-?1 signaling and as such might be an appropriate target for therapies to influence cardiac remodeling. äCaveolin-1 modulates TGF-?1 signaling in cardiac remodeling (epmc).pdf DeepDyve Pubget Overpricing