| Objective atrial fibrillation (AF) is the most common arrhythmia inclinical practice, and it is also a common cause of increased mortality. The riskof atrial fibrillation is directly related to the risk of death from stroke and heart failure. Atrial remodeling is the basis of the occurrence of atrial fibrillation,atrial fibrillation itself can promote reconstruction and increase the occurrence and development of atrial fibrillation. The occurrence of persistent atrialfibrillation is a chronic process based on tissue remodeling and electrical remodeling. Atrial structural remodeling in the most significant characteristics of atrial fibrosis, in chronic atrial fibrillation maintenance play an important role,delay of atrial structural remodeling can effectively prevent atrial fibrillation recurrence, in the treatment of atrial fibrillation has positive effect. TGF beta signaling is multifunctional pathway, is to start and terminate the tissue repair of key cytokines and also regulate the basis of tissue fibrosis and close relationship with atrial fibrillation. Tgfbr3 (transforming growth factor type III receptor,also known as betaglycan) as part of a TGF beta receptor, and is closely related to myocardial fibrosis, but the in the incidence of atrial fibrillation mechanism remains to be determined. This study will through the relationship between the patients with atrial fibrillation and atrial fibrosis and rat atrial myocytesintervention of tgfbr3 through the regulation of TGF beta signaling explore tgfbr3 in atrial fibrillation atrial fibrosis.Methods: (1) 104 cases of thoracic surgery were divided into atrial fibrillation group (43 cases) and sinus rhythm group (61 cases). Operation receives a small right atrial appendage tissue, morphological changes were observed by HE staining. Electron microscope was used to observe the ultrastructure changes,Masson staining was used to observe atrial collagen fibers deposition changes,real-time fluorescence quantitative PCR and Western blot detection of two groups of patients with right atrial appendage tgfbr3, Smad2, fibronectin (FN)mRNA and protein expression levels. (2) PCR and Western real-time fluorescence quantitative Blot detection of neonatal rat atrial myocytes of primary rat SD in different concentration and different time of TGF beta stimulated fibroblasts. (3) using siRNA interference technology, silencing and overexpression fiber cells in mRNA expression of osteoblasts in SD rat atrial and tgfbr3 regulation of TGF beta signaling pathway in atrial fibrosis in discussion of the role, for the study of mechanism of atrial fibrillation provides new ideas.Results of the study show: (1) expression of level (0.9672 + 0.5436) was significantly higher than that of the atrial fibrillation group 0.4718 + 0.3399, t=4.455, P < 0.05; real fibrillation group patients with right atrial appendage tgfbr3 protein expression level (0.7471 + 0.3990) in the significantly below the sinus rhythm group (1.2020 + 1.05783) sinus of patients with right atrial appendage tgfbr3 mRNA and T = 2.331, P < 0.05. Sinus of patients with right atrial appendage of Smad2 mRNA expression level (0.4615 + 0.2281), was significantly lower than that of the atrial fibrillation group 4.3095 + 0.1311, t=-1.483, P < 0.05; real fibrillation group patients with right atrial appendage of Smad2 protein expression level (1.2758 + 0.8141) was significantly higher than that in sinus rhythm group 0.8636 + 0.4795, t = 46.128 P < 0.05. Sinus rhythm group 1.5884 + 0.9480 higher than level (2.2621 + 1.6670), t =-2.093, P < 0.05;atrial fibrillation group fibronectin expression level (2.5122 + 1.9485) in the also were significantly higher than those in sinus rhythm group (1.5998 + 1.0376)real fibrillation group patients with right atrial appendage fibronectin mRNA expression and t =-2.268, P < 0.05. Smad2, Fibronectin expression levels were significantly increased, collagen expression increased. (2) Masson staining showed that the atrial fibrillation group, right atrial appendage collagen deposition was significantly more than that in sinus rhythm group.2. in vitro cytology experimental results: (1) lentiviral transfection of rat neonatal rat atrial into fiber cells to silence and over expression of tgfbr3 gene and have shown anti fibrosis effect of tgfbr3; (2) and TGF-? intervention in primary rat atrial into fiber cells results: TGF- ? promotes rat atria into fiber cells secreted fibronectin, and presenting the concentration dependence and time dependence, reduce tgfbr3 expression.The above results showed that down-regulation of TGFBR3 plays an important role in the process of atrial fibrosis in. The down-regulation of TGFBR3 TGF- ?enhanced signaling pathway promotes atrial fibroblasts secreting extracellular matrix, leading to atrial fibrosis. |
PDF Full Text Request