Effects Of Transforming Growth Factor-¦¢1 On Collagen Expression In Rat Atrial And Ventricular Fibroblasts
Keywords
Transforming Growth Factor Beta 1, Atrial Fibrillation, Collagen, Smads Proteins
Abstract
Objective To observe the different effects of transforming growth factor-¦Â1 (TGF-¦Â1) on collagen expression in rat atrial and ventricular fibroblasts, and to explore its possible molecular mechanisms. Methods: Rat primary atrial and ventricular fibroblasts were cultured using the tissue patch method, and the cells were identified by SABC immunocytochemical staining. The following experiments were performed: ¢Ù hydroxyproline digestion method was used to observe different concentrations of TGF-¦Â1 (0, 5, 10ng/ml) and different action times (6, 12, 24, 48h) on the hydroxyproline content of atrial and ventricular fibroblasts. ¢Ú Use the selected optimal intervention concentration and action time of TGF-¦Â1 to stimulate atrial and ventricular fibroblasts respectively. After Western blotting detects ¦Á-smooth muscle actin (¦Á-SMA) to identify myofibroblasts, use the hydroxyproline method to compare The expression of hydroxyproline in the two cell culture fluids, RT-PCR was used to detect the mRNA expression of type I and type III collagen, and Western blotting was used to detect the expression of Smad2/3, p-Smad2/3 and Smad7 proteins. Results TGF-¦Â1 could promote collagen synthesis in rat atrial and ventricular fibroblasts, and the effect was strongest when TGF-¦Â1 stimulation conditions were 5ng/ml and 24 hours. TGF-¦Â1 under the above conditions was used to stimulate atrial and ventricular fibroblasts. Compared with the control group, the expression of type I and III collagen and p-Smad2/3 in atrial fibroblasts increased and the expression of Smad7 decreased, and the difference was statistically significant (P <0.05); compared with the TGF-¦Â1 stimulation group of atrial fibroblasts and the TGF-¦Â1 stimulation group of ventricular fibroblasts, there was no statistically significant difference in the expression of Smad2/3 between the two groups, but the TGF-¦Â1 stimulation group of atrial fibroblasts ¢ñ , type III collagen, the expression of p-Smad2/3 was significantly increased, and the expression of Smad7 was significantly decreased (P<0.05). Conclusion TGF-¦Â1 can induce the transformation of cardiac fibroblasts into myofibroblasts, which can cause abnormal cellular collagen metabolism. The abnormality of collagen metabolism in atrial fibroblasts is more obvious than that in ventricular fibroblasts. The mechanism may be related to TGF-¦Â1/SMAD. related to signaling pathways. For further information of this article and research, feel free to contact our team for asssitance. Original research was done by Liu Fajin, Xiao Hua, Tang Xuejiao, Zhang Lei
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