Effect of microRNA-101 on atrial fibrosis in human chronic atrial fibrillation
10.3969/j.issn.1006-5725.2015.06.008
- VernacularTitle:微小RNA鄄101在心房颤动心房纤维化中的作用
- Author:
Zhiyuan JIANG
;
Guoqiang ZHONG
;
Fei XIAO
;
Yan HE
;
Yujie HONG
- Publication Type:Journal Article
- Keywords:
Atrial fibrillation;
microRNA-101;
Atrial fibrosis;
Transforming growth factor β typeⅠreceptor
- From:
The Journal of Practical Medicine
2015;(6):890-893
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of microRNA-101 (miRNA-101) on atrial fibrosis in human chronic atrial fibrillation (AF). Methods Right atrial appendages were obtained from 59 patients (30 with AF) undergoing cardiac surgery, including 47 patients with valve heart disease and 12 patients with congenital heart disease. The expression of miRNA-101 was determined by quantitative real-time PCR in the right atrial appendages of patients with and without AF. The cell-specific localization of miRNA-101 was detected by in situ hybridization assay. The mRNA and protein expression levels of transforming growth factor β typeⅠreceptor (TGFβRⅠ) and collagen type I (COL1) were determined by quantitative real-time PCR and Western-blot assay, respectively. Collagen in the right atrial appendages was observed by Masson staining assay. Results The expression of miRNA-101 was found to be significantly down-regulated in AF patients compared with patients with sinus rhythm (SR) (P < 0.05). The result of miRNA-ISH showed that miRNA-101, which was highly distributed within the connective tissues of heart, was down-regulated at about 24.9% in patients with AF compared with patients with SR. No significant differences at the mRNA expression level of TGFβRI was found between patients with AF and patients with SR (P > 0.05). But the protein expression of TGFβRI in patients with AF was significantly higher than that of patients with SR (P < 0.05). The mRNA and protein expressionsl of COL1 were significantly higher in patients with AF than thoset of patients with SR (P < 0.05). The collagen was significantly increased in patients with AF than that of patients with SR (P < 0.05). Conclusions Downregulation of miRNA-101 may contribute to atrial fibrosis in human atrial fibrillation by targeting TGFβRⅠ.
