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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: In this study, we observed the changes of trabecular cells cultured before and after dexamethasone treatment to investigate the mechanism of increased aqueous humor discharge resistance in steroid-induced glaucoma. METHODS: Human trabecular meshwork cells were cultured to near-high level of differentiation in vivo. Dexamethasone treatment followed by observation of the changes of cell morphology and detection of the following protein distribution and expression: (1) myocilin / TIGR protein; (2) fibronectin Protein; (3) actin cross-linked network formation; (4) serum amyloid A protein. RESULTS: After treated with dexamethasone, trabecular cells were enlarged, irregularly arranged and fuzzy boundaries were observed. (2) The expression of myocilin / TIGR protein in cells was significantly increased (3) the expression of fibronectin increased; (4) the formation of CLANs and the enhancement of intercellular connection; (5) the increase of serum amyloid A protein expression. Conclusion: The morphology of human trabecular meshwork cells treated with dexamethasone may be related to the change of stress fibers and the accumulation of myocilin protein in the cells. Intercellular boundary is unclear, and extracellular matrix protein overexpression, deposition. Trabecular meshwork extracellular matrix deposition and abnormal cell-cell connections and other changes in aqueous humor discharge resistance increased pathological process.