CAJ | 학술논문

目的：探索肌纤生成调节因子－1（ myofibrillogenesis regulator－1，MR－1）通过调节肌原纤维生成引起心肌肥大的机制。方法干预MR－1在体外培养的新生乳大鼠心肌细胞中的表达，检测心肌细胞表面积、心房利钠因子和脑钠肽水平及蛋白合成速率3种心肌肥大指标的变化，以鬼笔环肽－异硫氰酸荧光素标志并观察肌节F－actin组装，以半定量反转录－聚合酶链反应、免疫印迹和细胞免疫荧光术检测重要肌节分子myo－mesin－1、肌球蛋白调节轻链－2（ myosin light chain－2，MLC－2）含量及亚细胞定位。结果 MR－1过表达引起心肌细胞肥大、肌节F－actin组装明显促进、MLC－2与myomesin－1表达上调（ P＜0．05）以及myomesin－1的细胞核－细胞质转位；MR－1沉默后小泛素样调节因子－1过表达引起的转位和肌节F－actin组装明显抑制。结论 MR－1通过促进myomesin－1和MLC－2调节肌原纤维生成引起心肌细胞肥大。
목적：탐색기섬생성조절인자－1（ myofibrillogenesis regulator－1，MR－1）통과조절기원섬유생성인기심기비대적궤제。방법간예MR－1재체외배양적신생유대서심기세포중적표체，검측심기세포표면적、심방리납인자화뇌납태수평급단백합성속솔3충심기비대지표적변화，이귀필배태－이류청산형광소표지병관찰기절F－actin조장，이반정량반전록－취합매련반응、면역인적화세포면역형광술검측중요기절분자myo－mesin－1、기구단백조절경련－2（ myosin light chain－2，MLC－2）함량급아세포정위。결과 MR－1과표체인기심기세포비대、기절F－actin조장명현촉진、MLC－2여myomesin－1표체상조（ P＜0．05）이급myomesin－1적세포핵－세포질전위；MR－1침묵후소범소양조절인자－1과표체인기적전위화기절F－actin조장명현억제。결론 MR－1통과촉진myomesin－1화MLC－2조절기원섬유생성인기심기세포비대。
Objective Exploration of myofibrillogenesis reguiator-1 ( MR-1) by regulating the generation mechanism of causing myofibrillar hyperlrophy of the cardigmyocytes .Methods Af-ter intervention of MR-1 expressions in neonatal rat cardiomyocytes , we measured several hyper-trophic index e .g.the mRNA levels of the atrial natriuretic factor ( ANF) and brain natriuretic pep-tide ( BNP ) , the cell size , and the velocity of protein synthesis .The sarcomeric F-actin organization were detacted by staining with phalloidin-fluorescein isothiocyanate ( FITC);sublocation of myome-sin-1 and myosin regulatory light chain ( MLC-2) were assessed by semi-quantitative reverse tran-scription-polymerase chain reaction ( RT-PCR), western blot, and immunocytofluorescent assays . Results MR-1 overexpression induced cardiomyocyte hypertrophy , promoted the sarcomeric F-actin organization , increased the expression of MLC-2 and myomesin-1 ( P<0.05 ) , as well as the myome-sin-1 translocation from nucleus to cytoplasm .Those results of myomesin-1 translocation and F-actin organization were similar to the small ubiquitin modifier-1 ( SUMO-1) overexpression , MR-1 inhibi-tion by RNA interference did not induce the translocation of myomesin-1, even decrease the SUMO-1 overexpression induced myomesin-1 translocation , as well as the promoted F-actin organization . Conclusion MR-1 induces cardiomyocytes hypertrophy by promoting the MLC-2 and myomesin-1 induced myofibrillogenesis .