摘要
目的:原发性开角型青光眼(POAG)是一种发病隐匿的不可逆性致盲性眼病,发病机制有待进一步探讨。本研究通过电镜检测方法从小梁细胞线粒体形态改变及细胞连接的异常认识小梁细胞退行性改变,探讨POAG的发病机理。方法:原代培养POAG小梁网(GTM)与正常人的小梁网(NTM)细胞,电镜下对比观察小梁细胞线粒体和细胞连接的形态结构。结果:透射电镜可见培养的NTM细胞胞质内线粒体数量较多,结构完整,嵴的数目和形态正常,细胞连接以缝隙连接为主,结构完整,并可见丰富的粗面内质网,偶可见高尔基体等细胞器;GTM细胞线粒体数目少,形状多为空泡状,嵴多不可见,难以找到完整的细胞连接结构,其它细胞器明显减少。结论:(1)POAG患者小梁细胞的线粒体发生了病理学形态的退行性改变;(2)POAG患者小梁细胞的细胞连接连接出现了病理学形态的异常。提出POAG患者小梁细胞线粒体的形态与功能异常以及小梁细胞的细胞连接异常可能导致小梁网功能异常,推测其与眼压升高及POAG发病密切相关。
Objective： Primary open angle glaucoma （POAG） is a kind of insidious disease which results in irreversible loss of vision. The mechanism of POAG needs further investigation. The aim of this study is to explore the pathogenesis of POAG by the degeneration of trabecular meshwork（TM） using electron microscope （EM） method.Methods： TM from POAG （GTM） and non-diseased individuals （NTM） were cultured in vitro. Comparison of mitochondria and cell junction in TM cells were observed through transmission EM.Results： There were many complete mitochondria in the cytoplasm of NTM cells. Main cell junction was gap junction which has complete structure between NTM cells. Massive rough endoplasmic reticulum and few Golgi apparatus were seen. In GTM cells, number of mitochondria is decreased with incomplete structure. Normal cell junction was hardly seen. Other cell organelles were also decreased.Conclusion： The abnormalities of cell junction and mitochondrial morphology in TM cells may cause the dysfunction of trabecuhr meshwork, which was closely related with the elevated intraocular tension and the mechanism of POAG.
出处
《中国伤残医学》
2012年第3期4-8,共5页
Chinese Journal of Trauma and Disability Medicine
基金
国家自然科学基金项目(No.81100665)
陕西省科技厅项目(2011K14-02-07)
陕西省卫生厅项目(2010D56)
陕西省教育厅项目(2010JK807)资助
