中文摘要：

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（myosinlightchain-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.

英文摘要：

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 .