激素性青光眼房水排出阻力增加的机制探讨  

Mechanisms for Increased Resistance to Aqueous Humor Outflow in Glucocorticoid-induced Glaucoma

作　　者：谭娟[1] 曹桂群[2] 郭琳[3] 余曼[2] 崔敏[2] 闫乃红[2] 王宁利[3] 陈晓明[2] 刘旭阳[2] 

机构地区：[1]南华大学附二院眼科,湖南衡阳421000 [2]四川大学华西医院眼科眼科学研究室,四川成都610041 [3]首都医科大学同仁医院眼科

出　　处：《华西医学》2008年第1期67-69,共3页West China Medical Journal

基　　金：2005湖南省教委重点项目(湘财教指[2004]50号);2004年国家自然科学基金面上项目(编号:30471863)

摘　　要：目的:本研究通过观察经地塞米松处理前后培养的人小梁细胞的变化,探讨激素性青光眼房水排出阻力增加的机制。方法:将人类小梁细胞培养至接近体内的高分化状态,用地塞米松处理后,观察细胞形态的变化,并检测以下蛋白的分布和表达:(1)myocilin/TIGR蛋白;(2)纤连蛋白;(3)肌动蛋白交联网的形成;(4)血清淀粉样物质A蛋白。结果:人小梁细胞经地塞米松处理后(1)胞体变大,排列不规则,边界模糊,呈"融合"状;(2)细胞内外myocilin/TIGR蛋白表达均明显增加,其胞外表达与纤连蛋白位置一致,提示相互作用;(3)纤连蛋白表达增加;(4)CLANs形成,细胞间连接增强;(5)血清淀粉样物质A蛋白表达增加。结论:人类小梁细胞经地塞米松处理后形态发生变化,可能与应力纤维变化及myocilin蛋白在细胞内积聚有关。细胞间边界不清,与细胞外基质蛋白过度表达、沉积有关。小梁细胞外基质沉积以及异常的细胞间连接等改变与房水排出阻力增加的病理过程有关。Objective：To determine the mechanism of glucocorticoid glaucoma by observing the changes of human trabecular meshwork（HTM）cell in culture treated with dexamethasone.Methods：HTM cells were cultured to a highly differentiated state and then were treated with dexamethasone.The changes in cell morphology were observed,then the distribution and expression of the following proteins were detected：（1）myocilin/TIGR,（2）fibronectin,（3）the formation of cross-linked actin（cross linked actin network,CLANs）,and（4）serum amyloid A（SAA）.Results：The changes of HTM cells after DEX treatment included：（1）morphology：the cell became bigger and irregular,the cell boundaries appeared to be＂fused＂,（2）protein expression showed：increased expression of the following proteins was determined：myocilin/TIGR,fibronectin,viculin,actin（CLANs formed）and SAA.Conclusion：The morphological changes of human trabecular cells after dexamethasone treatment might be correlated with the accumulation of stress fibers and myocilin protein in cells.The over-expression of extracellular matrix proteins caused fuzzy cell boundary.

关 键 词：青光眼 糖皮质激素 myocilin/TIGR蛋白 纤连蛋白 肌动蛋白交联网 血清淀粉样物质A 

分 类 号：R775[医药卫生—眼科]