中文摘要：

心肌肥大是心肌细胞面对多种病理刺激时的共同反应，以心肌细胞体积增大和胚胎期基因的重新表达为标志．心肌发育调控基因肌肉LIM蛋白（muscle LIM protein，MLP）的表达异常与心肌肥大有关．为研究MLP参与心肌肥大发生的分子机制，采用去氧肾上腺素（phenylephrine，PE）刺激大鼠原代培养心肌细胞，建立心肌细胞肥大模型，采用RNAi技术敲减MLP的表达，分析MLP与肥大信号通路钙调神经磷酸酶（calcineurin）／活化T细胞核因子（nuclearfactor of activated T-cells，NFAT）的关系．结果显示，原代培养的心肌细胞经一定浓度的PE刺激后细胞表面积增加，肥大标志蛋白ANP、BNP表达增高，并伴有MLP表达上调．RNAi方法敲减MLP的表达则明显抑制PE诱导的心肌细胞表面积增加和BNP表达增高，并且直接影响NFAT的转录激活活性，提示MLP与心肌肥大的发生密切相关，并且可能是通过calcineurin／NFAT信号通路而参与心肌肥大的发生．

英文摘要：

In response to numerous pathologic stimuli, the cardiomyocytes undergo a hypertrophic response characterized by increased myocardial cell size and activation of fetal cardiac genes. The abnormal expression of myocardium developing factor muscle LIM protein （MLP） contributes to this process. To investigate the mechanism of MLP participates in cardiac hypertrophy, we used phenylephrine （PE） to induce hypertrophic response in cultured rat neonatal ventricular myocytes and down-regulated expression of MLP with RNA interference. The relation between MLP and ealeineurin/ nuclear factor of activated T-cells （NFAT） signaling pathway was analyzed. Increased cell area and expression of ANP, BNP was observed in PE stimulated cardiomyocytes. Down-regulation of expression of MLP by RNA interference significantly inhibited PE induced hypertrophic response. Further more, activation of calcineurin/NFAT signaling pathway was reduced in MLP RNA interfered myocytes after PE stimulation. These results indicate that MLP is intimately involved the process of cardiac hypertrophy and possibly regulates this process through calcineurin/NFAT signaling pathway.