共同性内斜视患者眼外肌中肌球蛋白重链表达的研究

Expression of myosin heavy chain in extraocular muscles of patients with concomitant esotropia

目的探讨共同性内斜视的病理机制,探索斜视患者眼外肌的变化在其发病和治疗中的作用。方法对62例共同性内斜视患者及14例正常人眼外肌进行分子生物学分析,分离差异蛋白,质谱分析差异蛋白,Western blotting鉴定质谱测序结果 ;随机抽取6例共同性内斜视患者的外直肌,RT-PCR法检测肌球蛋白重链（myosin heavychain,MyHC）异构体-眼肌型（MYH13）在眼外肌中的表达。结果同正常对照相比,共同性内斜视患者的外直肌有12种蛋白表达差异（M1-M12）,将这些蛋白进行质谱测序分析得到以MyHC为主的收缩蛋白的缺失。Western blotting结果显示,共同性内斜视患者的眼外肌中不表达MyHC。RT-PCR结果显示,随机的6例共同性内斜视眼外肌中MYH13mRNA的表达水平分别为0.001±0.001、0.087±0.001、0.079±0.019、0.158±0.048、0.009±0.001、0.149±0.047,正常对照为1.000。MYH13mRNA在共同性内斜视的眼外肌中的表达与正常对照相比,差异均有统计学意义（均为P〈0.05）。结论 MyHC及MYH13在共同性内斜视患者眼外肌中表达缺失,是共同性内斜视发生、发展的主要原因之一。

Objective To evaluate the pathological mechanisms of concomitant esotropia and explore the effect of extraocular muscles on its pathogenesis and treatment.MethodsWe analyzed lateral rectus（LR）of 62 patients with concomitant esotropia and 14 normal humans by separating different proteins and mass spectrometry.Western blotting was used to detect the change of myosin heavy chain（MyHC）expression.Six LR from concomitant esotropia were randomly selected and real-time quantitative PCR was used for measurement of the change of eom-MyHC isoform expression.ResultsCompared with normal control group,M1-M12 protein bands absented or presented in the case group.And the change of contractile proteins of muscle such as myosin heavy chain was analyzed by mass spectrometry.Western blotting showed that expression of MyHC was not found in LR of patients with concomitant esotropia.Expressions of MYH13 mRNA of LR were 0.001±0.001,0.087±0.001,0.079±0.019,0.158±0.048,0.009±0.001,0.149±0.047 in randomly selected 6 cases with concomitant esotropia,and 1.000 for normals.There were statistical differences in expression of MYH13 mRNA of LR between concomitant esotropia patients and normals（all P0.05）.ConclusionAbsent of MyHC and MYH13 are found in LR of patients with concomitant esotropia,which is one of the main reasons for development of concomitant esotropia.