Identification of Differentially Expressed Genes Induced by Angiotensin Ii in Rat Cardiac Fibroblasts

Abstract

1. Cardiac fibroblasts play an important regulatory role in cardiac remodelling by undergoing proliferation, differentiation and upregulating various gene products, including some cytokines and extracellular matrix (ECM) proteins. A highly potent mediator of cardiac remodelling is angiotensin (Ang) II. 2. In the present study, the suppression subtractive hybridization method was used to identify differentially expressed cDNAs in adult rat cardiac fibroblasts induced by AngII. 3. Following mRNA isolation of non-stimulated and AngII-stimulated cells, cDNAs of both populations were prepared and subtracted by suppression polymerase chain reaction. Sequencing of the partially enriched cDNAs identified 36 genes differentially expressed, including ECM proteins (pro-alpha(1) collagen type III, fibronectin), structural protein (spectrin), enzyme (GTP-specific succinyl-CoA synthetase), transcriptional regulators (glucocorticoid-induced leucine zipper, inhibitor of DNA binding 3) and proteins involved in cell division control (cdc2) or cell signalling (insulin-like growth factor binding protein-3, mutant p53-binding protein, grp75, CGI-121, protein phosphatase type 2A, tspan-2 and Sam68). 4. The diversity of genes identified in the present study further emphasises the central role of AngII in the regulation of cardiac remodelling.

Betulinic acid prevents high glucose-induced expression of extracellular matrix protein in cardiac fibroblasts by inhibiting the TGF-β1/Smad signaling pathway

“…The differentiation of CFs into myofibroblasts and the exclusive deposition of ECM components, including α-SMA, collagen and fibronectin, are essential for the development of cardiac fibrosis (20). Previous evidence has suggested that the differentiation of CFs occurs in response to high glucose, TGF-β1 and angiotensin-II, which are important in this process (21,22). In the present study, it was found that the expression of α-SMA was significantly increased by high glucose.…”

Genome-Wide Association of New-Onset Hypertension According to Renin Concentration: The Korean Genome and Epidemiology Cohort Study

“…Increased preload can result in vessel injury and cardiac remodeling. Therefore, the RAS is down-regulated, and the SPTAN1 gene is activated for compensation for vessel fibrosis [60].…”

Qiliqiangxin inhibits angiotensin II‐induced transdifferentiation of rat cardiac fibroblasts through suppressing interleukin‐6

“…AngII, the one of most important renin‐angiotensin system components, played a critical role in cardiac remodelling. Recently investigations focused its impact on CFs transdifferentiation . Because, CFs conversion into myofibroblasts resulted in collagen production and deposition, which might increase the risk of myocardial fibrosis and remodelling .…”

“…Recent studies demonstrated that Angiotensin II (AngII) plays a important role in fibroblasts differentiation , and AngII is also critically involved in chronic inflammation and progessive fibrosis during pressure overload . AngII infusion significantly increased Interleukin‐6(IL‐6) expression in rats’ heart, meanwhile elevated IL‐6 serum levels promoted cardiac fibrosis through TGF‐β 1 /Smad (TGF‐β 1 /Smad) signalling pathway , and promoting transdifferentiation of CFs into myofibroblasts .…”