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Nox2 contributes to cardiac fibrosis in diabetic cardiomyopathy in a transforming growth factor-? dependent manner |pdf=|usr=}}{{26617806}} gab.com Text Nox2 contributes to cardiac fibrosis in diabetic cardiomyopathy in a transforming growth factor- dependent manner JO: Int J Clin Exp Pathol http://www.kidney.de/pget.php?&tw=1&pmid=26617806 #FOAvip Purpose: This study aimed to investigate the effect of Nox2 on cardiac fibrosis and to elucidate the regulatory mechanism of Nox2 in the development of DCM. Methods: We established normal and insulin-resistant cellular model using neonatal rat cardiac fibroblasts. Then Nox2-specific siRNA were transfected into cardiac fibroblasts with Lipofectamine ® 2000 and crambled siRNA sequence was considered as control. Meanwhile, a part of cells were randomly selected to be treated with or without transforming growth factor-? (TGF-?). Moreover, quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were respectively performed to determine the expression level of related molecules, such as Nox2, collagen type I and III (COL I and III) and PI3K/AKT and PKC/Rho signaling pathway-related proteins. Results: TGF-? stimulation significantly increased the expression level of Nox2 both in mRNA and protein levels. Suppression of the Nox2 markedly decreased the expression of COL I and COL III in normal and insulin-resistant cellular model with TGF-? stimulation. Moreover, suppression of the Nox2 significantly decreased the expression of PI3K/AKT and PKC/Rho signaling pathway-related proteins in insulin-resistant cellular model with TGF-? stimulation. However, suppression of Nox2 had no effects on these proteins without TGF-? stimulation. Conclusions: Our finding reveals that Nox2 may promote synthesis of COL I and III via involved in PI3K/AKT and PKC/Rho signaling pathway in a TGF-? dependent manner and consequently promote cardiac fibrosis in the development of DCM. Twit Text FOAVip Nox2 contributes to cardiac fibrosis in diabetic cardiomyopathy in a transforming growth factor- dependent manner ????Int J Clin Exp Pathol http://www.kidney.de/pget.php?&tw=1&pmid=26617806 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26617806 #FOAvip English Wikipedia <ref>{{Cite pmid|26617806}}</ref> Nox2 contributes to cardiac fibrosis in diabetic cardiomyopathy in a transforming growth factor-? dependent manner #MMPMID26617806 Liu Y; Zhang J Int J Clin Exp Pathol 2015[]; 8 (9): 10908-14 PMID26617806show ga Purpose: This study aimed to investigate the effect of Nox2 on cardiac fibrosis and to elucidate the regulatory mechanism of Nox2 in the development of DCM. Methods: We established normal and insulin-resistant cellular model using neonatal rat cardiac fibroblasts. Then Nox2-specific siRNA were transfected into cardiac fibroblasts with Lipofectamine ® 2000 and crambled siRNA sequence was considered as control. Meanwhile, a part of cells were randomly selected to be treated with or without transforming growth factor-? (TGF-?). Moreover, quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were respectively performed to determine the expression level of related molecules, such as Nox2, collagen type I and III (COL I and III) and PI3K/AKT and PKC/Rho signaling pathway-related proteins. Results: TGF-? stimulation significantly increased the expression level of Nox2 both in mRNA and protein levels. Suppression of the Nox2 markedly decreased the expression of COL I and COL III in normal and insulin-resistant cellular model with TGF-? stimulation. Moreover, suppression of the Nox2 significantly decreased the expression of PI3K/AKT and PKC/Rho signaling pathway-related proteins in insulin-resistant cellular model with TGF-? stimulation. However, suppression of Nox2 had no effects on these proteins without TGF-? stimulation. Conclusions: Our finding reveals that Nox2 may promote synthesis of COL I and III via involved in PI3K/AKT and PKC/Rho signaling pathway in a TGF-? dependent manner and consequently promote cardiac fibrosis in the development of DCM. äNox2 contributes to cardiac fibrosis in diabetic cardiomyopathy in a t(epmc).pdf DeepDyve Pubget Overpricing