LncRNA NRON Alleviates Atrial Fibrosis Via Promoting NFATc3 Phosphorylation

Background: atrial fibrillation(atrial fibrillation,AF)as one of the clinical significance of arrhythmia,is a risk factor for thrombosis and heart failure.The development of atrial fibrosis is a sign of structural modification and is considered to be a key factor leading to the development of AF.AF occurs due to the electrical remodeling and atrial remodeling caused by ion channel abnormalities and atrial fibrosis,and AF then deepens the degree of electrical remodeling and atrial remodeling,and the interaction between the two results in the continuous aggravation of the patient's condition.With the deepening of AF research in recent years,the latest evidence has found that long non-coding ribonucleic acid(Lnc RNA),including CHRF,H19,MIAT and so on,has abnormal expression in myocardial fibrosis.Lnc RNA is a group of non-protein-coding RNA molecules.Multiple studies have shown that there are a variety of lncrnas in the heart and vascular system,and these lncrnas have certain regulatory effects on biological processes,but the relationship between Lnc RNA and AF has not been explored.Of Lnc RNA NRON was shown to inhibit T cell activation factor(Nuclear factor of activated T cells,NFAT)expression,at the same time existing experiments confirmed that calmodulin calcineurin/NFAT signal pathways in cardiac hypertrophy and fibrosis plays an important role,therefore proven NRON role in the process of atrial fibrosis may give clinicians in identifying high-risk AF and promptly take effective treatment to provide new ideas.Objective: to explore the specific mechanism of LncRNA NRON affecting NFAT activity and progression of atrial fibrosis.Methods: the expression level of NRON in atrial tissue was detected by qrt-pcr.Western blotting was used to determine the protein levels of collagen I,collagen III,NFATc3 and p NFATc3.Immunohistochemistry was performed to observe the expression and distribution of collagen I in atrial tissue.Atrial fibroblasts were identified by vimentin/troponin immunofluorescence staining.Then the proliferation of fibroblasts was detected by cck-8 analysis.HE staining was used to observe the morphological changes of cardiac tissue,and finally the myocardial fibrosis was detected by Masson staining.Results: NRON expression was significantly down-regulated in AF compared with SR.NRON inhibits fibroblast proliferation;Expression of collagen I and collagen III;Activate NFATc3 and nuclide entry.Overexpression of NRON inhibited the cardiac fibrosis induced by ang-ii in mice.Conclusions: the data from this study suggest that NRON alleviates atrial fibrosis by promoting NFATc3 phosphorylation.