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10.1177/1470320318759358 http://scihub22266oqcxt.onion/10.1177/1470320318759358 C5888824!5888824 !29575960     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29575960 &cmd=llinks): Failed to open stream: HTTP request failed! 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Connective tissue growth factor expression after angiotensin II exposure is dependent on transforming growth factor-? signaling via the canonical Smad-dependent pathway in hypertensive induced myocardial fibrosis |pdf=|usr=}}{{29575960 }} gab.com Text Connective tissue growth factor expression after angiotensin II exposure is dependent on transforming growth factor- signaling via the canonical Smad-dependent pathway in hypertensive induced myocardial fibrosis JO: J Renin Angiotensin Aldosterone Syst http://www.kidney.de/pget.php?&tw=1&pmid=29575960 #FOAvip INTRODUCTION: Transforming growth factor-? (TGF-?) and connective tissue growth factor (CTGF) are often described as the initial pro-fibrotic mediators upregulated early in fibrosis models dependent on angiotensin II (Ang-II). In the present study, we explore the mechanistic link between TGF-? and CTGF expression by using a novel TGF-? trap. MATERIALS AND METHODS: NIH/3T3 fibroblasts were subjected to TGF-? with or without TGF-? trap or 1D11 antibody, CTGF or CTGF plus TGF-? for six or 24 hours, and then used for quantitative real-time polymerase chain reaction (qRT-PCR) or immunocytochemistry. Male C57BL/6 mice were infused with Ang-II and randomly assigned TGF-? trap for six or 24 hours. Hearts were harvested for histological analyses, qRT-PCR and western blotting. RESULTS: Exogenous TGF-?-induced fibroblasts resulted in significant upregulation of CTGF, TGF-? and type I collagen transcript levels in vitro. Additionally, TGF-? promoted the differentiation of fibroblasts into ?-SMA(+) myofibroblasts. CTGF expression was reduced by the addition of TGF-? trap or neutralizing antibody, confirming that its expression is dependent on TGF-? signaling. In contrast, exogenous CTGF did not appear to have an effect on fibroblast production of pro-fibrotic transcripts or fibroblast differentiation. Ang-II infusion in vivo led to a significant increase in TGF-? and CTGF mRNA expression at six and 24 hours with corresponding changes in Smad2 phosphorylation (pSmad2), indicative of increased TGF-? signaling. Ang-II animals that received the TGF-? trap demonstrated reduced CTGF mRNA levels and pSmad2 at six hours, suggesting that early CTGF expression is dependent on TGF-? signaling. CONCLUSIONS: We demonstrated that CTGF expression is dependent on TGF-? signaling both in vitro and in vivo in a model of myocardial fibrosis. This also suggests that early myocardial CTGF mRNA expression (six hours) after Ang-II exposure is likely dependent on latent TGF-? activation via the canonical Smad-dependent pathway in resident cardiac cells. Twit Text FOAVip Connective tissue growth factor expression after angiotensin II exposure is dependent on transforming growth factor- signaling via the canonical Smad-dependent pathway in hypertensive induced myocardial fibrosis ????J Renin Angiotensin Aldosterone Syst http://www.kidney.de/pget.php?&tw=1&pmid=29575960 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29575960 #FOAvip English Wikipedia <ref>{{Cite pmid|29575960 }}</ref> Connective tissue growth factor expression after angiotensin II exposure is dependent on transforming growth factor-? signaling via the canonical Smad-dependent pathway in hypertensive induced myocardial fibrosis #MMPMID29575960 Wong CKS ; Falkenham A ; Myers T ; Légaré JF J Renin Angiotensin Aldosterone Syst 2018[Jan]; 19 (1 ): 1470320318759358 PMID29575960 show ga INTRODUCTION: Transforming growth factor-? (TGF-?) and connective tissue growth factor (CTGF) are often described as the initial pro-fibrotic mediators upregulated early in fibrosis models dependent on angiotensin II (Ang-II). In the present study, we explore the mechanistic link between TGF-? and CTGF expression by using a novel TGF-? trap. MATERIALS AND METHODS: NIH/3T3 fibroblasts were subjected to TGF-? with or without TGF-? trap or 1D11 antibody, CTGF or CTGF plus TGF-? for six or 24 hours, and then used for quantitative real-time polymerase chain reaction (qRT-PCR) or immunocytochemistry. Male C57BL/6 mice were infused with Ang-II and randomly assigned TGF-? trap for six or 24 hours. Hearts were harvested for histological analyses, qRT-PCR and western blotting. RESULTS: Exogenous TGF-?-induced fibroblasts resulted in significant upregulation of CTGF, TGF-? and type I collagen transcript levels in vitro. Additionally, TGF-? promoted the differentiation of fibroblasts into ?-SMA(+) myofibroblasts. CTGF expression was reduced by the addition of TGF-? trap or neutralizing antibody, confirming that its expression is dependent on TGF-? signaling. In contrast, exogenous CTGF did not appear to have an effect on fibroblast production of pro-fibrotic transcripts or fibroblast differentiation. Ang-II infusion in vivo led to a significant increase in TGF-? and CTGF mRNA expression at six and 24 hours with corresponding changes in Smad2 phosphorylation (pSmad2), indicative of increased TGF-? signaling. Ang-II animals that received the TGF-? trap demonstrated reduced CTGF mRNA levels and pSmad2 at six hours, suggesting that early CTGF expression is dependent on TGF-? signaling. CONCLUSIONS: We demonstrated that CTGF expression is dependent on TGF-? signaling both in vitro and in vivo in a model of myocardial fibrosis. This also suggests that early myocardial CTGF mRNA expression (six hours) after Ang-II exposure is likely dependent on latent TGF-? activation via the canonical Smad-dependent pathway in resident cardiac cells. |*Signal Transduction/drug effects [MESH] |Angiotensin II/*pharmacology [MESH] |Animals [MESH] |Cell Differentiation/drug effects [MESH] |Connective Tissue Growth Factor/genetics/*metabolism [MESH] |Fibrosis [MESH] |Hypertension/*metabolism [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Myocardium/*metabolism/*pathology [MESH] |Myofibroblasts/drug effects/metabolism/pathology [MESH] |NIH 3T3 Cells [MESH] |Phosphorylation/drug effects [MESH] |RNA, Messenger/genetics/metabolism [MESH] |Smad Proteins/*metabolism [MESH] |Transforming Growth Factor beta/genetics/*metabolism [MESH]Connective tissue growth factor expression after angiotensin II exposu(epmc).pdf DeepDyve Pubget Overpricing