| The research backgroundFibrosis is a pathological change, which occurs in a variety of organs, shows that the fibrous connective tissue increased and the parenchymal cells decreased, the continuous progress can cause the organ damage and functional decline or even failure. Atrial fibrosis, refers to the abnormal collagen deposition in atrial interstitial cells, leading to the atrial structural remodeling and the electrophysiological remodeling, which causes atrial fibrillation(AF). Fibrillation, the most common arrhythmia, often accompanied by heart room fibrosis. A number of studies of atrial fibrillation (af) animal models and clinical atrial fibrillation has authenticated, atrial fibrillation and atrial structure and electric transformation progress. Is a kind of atrial remodeling organization structure changes, including the apoptosis, necrosis, atrium expansion and fibrosis. And the atrial fibrosis is one of the important pathologic basis of atrial remodeling in atrial fibrillation.Caveolae Was first reported as early as in the middle of last century. Over the past decade, research has already developed into a rapid expansion of field, and alveolus has been identified as one of the important members transcytosis macromolecules, cholesterol transport and signal transduction in various types of cells. Caveolin-1, the first member of the alveolus gene family structure composed of three related protein:(Cav) Caveolin Caveolin-1-2-2 (of Cav) and Caveolin-3 (Cav-3). Cav 1 fossa organelles of the cells of main structure parts. In the cardiovascular system, and Cav Cav-1-2 of a variety of cells and tissue types, but one of the most abundant fibroblasts and endothelial cells, and Cav-3 strict expression of myocardial cells.The purine receptor family is found in one of the most complex receptor families, which is widely distributed in our bodies. There are 7 kinds of P2X receptors, belonging to the ATP gating ion channel receptors. And the study of the receptors were relatively extensive in antoimmune diseases. A new study found that P2X7R existed in the lipid rafts of the atrial tissue in vivo and in vitro, and composed a protein complex with Cav-1,-3. The three ones raised or lowered to maintain the dynamic balance of the complex, which may become an important control point if the cardiovascular pathological process. The experiment was mainly to study the expression of the caveolin and P2X7R in the atrial fibrosis.Research purpose:Study change of Cav-1/Cav-3/P2X7 receptors in atrial fibrosis atrial fibrosisatrial fibrillation patients.Materials and Methods:1. PatientsThe subjects included 69, rheumatic heart disease mitral or aortic valve replacement June 1,2013 to December 30,2014.45 were diagnosed with af (experimental group) and 24 no history of atrial fibrillation (control group). After written informed consent, atrial tissue samples from the right atrium attachment by all subjects. Sample is used in the main culture of human atrial fibroblasts, or frozen and stored in a-80 ℃ for western blot protein extraction, or neutralize 10% formalin fixed tissue pathology analysis.2. Cell cultureHuman atrial fibroblasts (the framework) from the biopsy of the right atrium in the attachment. Channel 2-4 cells were plated in 6-well plate. Serum is cancellation 24 hours before hatching with recombinant human TGF-beta 148 h, and then hatch 48 h with or without 100 ng/ml TGF-beta 1. From each group cells then harvested for western blot analysis.3. Statistical analysisThe result means+SE. Determine the use of the difference between group t. Statistical test double tail, p-value< 0.05. Statistical analysis with SPSS 16.0 software (SPSS, Chicago, IL).Results:The study indicated the downregulation of atrial Cav-1 and the overexpression of Cav-3/P2X7 receptor of atrial fibrosis in AF patients. Western blot analyses showed Cav 1 the protein content of about 30% in atrial fibrillation subjects is lower than the control group (P< 0.001).Conculsion:Our study suggested the downregulation of Cav-1 and the overexpression of Cav-3/P2X7Receptor is an important regulator of atrial fibrillation and a promising target for the treatment of atrial fibrillation. |
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