AI Article Synopsis
- The study investigates how Nox2 contributes to cardiac fibrosis and its regulatory mechanisms in diabetic cardiomyopathy (DCM).
- Using neonatal rat cardiac fibroblasts, researchers applied siRNA to target Nox2 and measured the effects on collagen types I and III, as well as related signaling pathways, particularly with and without TGF-β treatment.
- Results indicate that TGF-β boosts Nox2 expression, which in turn enhances collagen production and activates specific signaling pathways, suggesting Nox2 plays a key role in promoting cardiac fibrosis in DCM.
Article Abstract
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-β (TGF-β). 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-β 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-β 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-β stimulation. However, suppression of Nox2 had no effects on these proteins without TGF-β 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-β dependent manner and consequently promote cardiac fibrosis in the development of DCM.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4637621 | PMC |
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