Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1042/CS20120636 http://scihub22266oqcxt.onion/10.1042/CS20120636 C4075193!4075193!23841699     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 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Clin+Sci+(Lond) 2014 ; 126 (4): 275-88 Nephropedia Template TP {{tp|p=23841699|t=2014. Fibulin-2 deficiency attenuates angiotensin II-induced cardiac hypertrophy by reducing transforming growth factor-? signalling |pdf=|usr=}}{{23841699}} gab.com Text Fibulin-2 deficiency attenuates angiotensin II-induced cardiac hypertrophy by reducing transforming growth factor- signalling JO: Clin Sci (Lond) http://www.kidney.de/pget.php?&tw=1&pmid=23841699 #FOAvip AngII (angiotensin II) is a potent neurohormone responsible for cardiac hypertrophy, in which TGF (transforming growth factor)-? serves as a principal downstream mediator. We recently found that ablation of fibulin-2 in mice attenuated TGF-? signalling, protected mice against progressive ventricular dysfunction, and significantly reduced the mortality after experimental MI (myocardial infarction). In the present study, we investigated the role of fibulin-2 in AngII-induced TGF-? signalling and subsequent cardiac hypertrophy. We performed chronic subcutaneous infusion of AngII in fibulin-2 null (Fbln2?/? ), heterozygous (Fbln2+/? ) and WT (wild-type) mice by a mini-osmotic pump. After 4 weeks of subpressor dosage of AngII infusion (0.2 ?g/kg of body weight per min), WT mice developed significant hypertrophy, whereas the Fbln2?/? showed no response. In WT, AngII treatment significantly up-regulated mRNAs for fibulin-2, ANP (atrial natriuretic peptide), TGF-?1, Col I (collagen type I), Col III (collagen type III), MMP (matrix metalloproteinase)-2 and MMP-9, and increased the phosphorylation of TGF-?-downstream signalling markers, Smad2, TAK1 (TGF-?-activated kinase 1) and p38 MAPK (mitogen-activated protein kinase), which were all unchanged in AngII-treated Fbln2?/? mice. The Fbln2+/? mice consistently displayed AngII-induced effects intermediate between WT and Fbln2?/? . Pressor dosage of AngII (2 mg/kg of body weight per min) induced significant fibrosis in WT but not in Fbln2?/? mice with comparable hypertension and hypertrophy in both groups. Isolated CFs (cardiac fibroblasts) were treated with AngII, in which direct AngII effects and TGF-?-mediated autocrine effects was observed in WT. The latter effects were totally abolished in Fbln2?/? cells, suggesting that fibulin-2 is essential for AngII-induced TGF-? activation. In conclusion our data indicate that fibulin-2 is essential for AngII-induced TGF-?-mediated cardiac hypertrophy via enhanced TGF-? activation and suggest that fibulin-2 is a potential therapeutic target to inhibit AngII-induced cardiac remodelling. Twit Text FOAVip Fibulin-2 deficiency attenuates angiotensin II-induced cardiac hypertrophy by reducing transforming growth factor- signalling ????Clin Sci (Lond) http://www.kidney.de/pget.php?&tw=1&pmid=23841699 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23841699 #FOAvip English Wikipedia <ref>{{Cite pmid|23841699}}</ref> Fibulin-2 deficiency attenuates angiotensin II-induced cardiac hypertrophy by reducing transforming growth factor-? signalling #MMPMID23841699 ZHANG H; Wu J; DONG H; KHAN SA; CHU ML; TSUDA T Clin Sci (Lond) 2014[Feb]; 126 (4): 275-88 PMID23841699show ga AngII (angiotensin II) is a potent neurohormone responsible for cardiac hypertrophy, in which TGF (transforming growth factor)-? serves as a principal downstream mediator. We recently found that ablation of fibulin-2 in mice attenuated TGF-? signalling, protected mice against progressive ventricular dysfunction, and significantly reduced the mortality after experimental MI (myocardial infarction). In the present study, we investigated the role of fibulin-2 in AngII-induced TGF-? signalling and subsequent cardiac hypertrophy. We performed chronic subcutaneous infusion of AngII in fibulin-2 null (Fbln2?/? ), heterozygous (Fbln2+/? ) and WT (wild-type) mice by a mini-osmotic pump. After 4 weeks of subpressor dosage of AngII infusion (0.2 ?g/kg of body weight per min), WT mice developed significant hypertrophy, whereas the Fbln2?/? showed no response. In WT, AngII treatment significantly up-regulated mRNAs for fibulin-2, ANP (atrial natriuretic peptide), TGF-?1, Col I (collagen type I), Col III (collagen type III), MMP (matrix metalloproteinase)-2 and MMP-9, and increased the phosphorylation of TGF-?-downstream signalling markers, Smad2, TAK1 (TGF-?-activated kinase 1) and p38 MAPK (mitogen-activated protein kinase), which were all unchanged in AngII-treated Fbln2?/? mice. The Fbln2+/? mice consistently displayed AngII-induced effects intermediate between WT and Fbln2?/? . Pressor dosage of AngII (2 mg/kg of body weight per min) induced significant fibrosis in WT but not in Fbln2?/? mice with comparable hypertension and hypertrophy in both groups. Isolated CFs (cardiac fibroblasts) were treated with AngII, in which direct AngII effects and TGF-?-mediated autocrine effects was observed in WT. The latter effects were totally abolished in Fbln2?/? cells, suggesting that fibulin-2 is essential for AngII-induced TGF-? activation. In conclusion our data indicate that fibulin-2 is essential for AngII-induced TGF-?-mediated cardiac hypertrophy via enhanced TGF-? activation and suggest that fibulin-2 is a potential therapeutic target to inhibit AngII-induced cardiac remodelling. äFibulin-2 deficiency attenuates angiotensin II-induced cardiac hypertr(epmc).pdf DeepDyve Pubget Overpricing