CAJ | 학술논문

目的：探讨微小RNA-101（miRNA-101）在心房颤动心房纤维化中的作用。方法：59例开胸手术患者（心脏瓣膜病47例，先天性心脏病12例），分为房颤组30例、窦律组29例。qPCR及锁定核苷酸原位杂交技术检测两组右心耳 miRNA-101表达；qPCR 检测两组右心耳转化生长因子βⅠ型受体（ TGFβRⅠ）、Ⅰ型胶原（COL1）mRNA 表达；免疫印迹法检测两组右心耳 TGFβRI、COL1蛋白表达；Masson 染色观察两组右心耳胶原的沉积。结果：房颤组右心耳 miRNA-101表达明显低于窦律组（P ＜0．05），原位杂交显示miRNA-101主要分布于心房结缔组织，房颤组 miRNA-101表达较窦律组下降24．9％；房颤组 TGFβRⅠmRNA表达与窦律组无明显差异（P ＞0．05），但蛋白表达明显高于窦律组（P ＜0．05）；COL1mRNA及蛋白表达均明显高于窦律组（P ＜0．05）；房颤组右心耳胶原沉积明显多于窦律组（P ＜0．05）。结论：miRNA-101下调在心房颤动心房纤维化过程中起重要作用，其可能通过调控TGFβRⅠ而参与心房纤维化。
목적：탐토미소RNA-101（miRNA-101）재심방전동심방섬유화중적작용。방법：59례개흉수술환자（심장판막병47례，선천성심장병12례），분위방전조30례、두률조29례。qPCR급쇄정핵감산원위잡교기술검측량조우심이 miRNA-101표체；qPCR 검측량조우심이전화생장인자βⅠ형수체（ TGFβRⅠ）、Ⅰ형효원（COL1）mRNA 표체；면역인적법검측량조우심이 TGFβRI、COL1단백표체；Masson 염색관찰량조우심이효원적침적。결과：방전조우심이 miRNA-101표체명현저우두률조（P ＜0．05），원위잡교현시miRNA-101주요분포우심방결체조직，방전조 miRNA-101표체교두률조하강24．9％；방전조 TGFβRⅠmRNA표체여두률조무명현차이（P ＞0．05），단단백표체명현고우두률조（P ＜0．05）；COL1mRNA급단백표체균명현고우두률조（P ＜0．05）；방전조우심이효원침적명현다우두률조（P ＜0．05）。결론：miRNA-101하조재심방전동심방섬유화과정중기중요작용，기가능통과조공TGFβRⅠ이삼여심방섬유화。
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.