首页 | 本学科首页   官方微博 | 高级检索  
     


Overexpression of myocilin in cultured human trabecular meshwork cells
Authors:Wentz-Hunter Kelly  Shen Xiang  Okazaki Kazushiro  Tanihara Hidenobu  Yue Beatrice Y J T
Affiliation:Department of Ophthalmology and Visual Sciences, University of Illinois at Chicago College of Medicine, Chicago, IL 60612, USA.
Abstract:The trabecular meshwork, a specialized eye tissue, is a major site for regulation of the aqueous humor outflow. Malfunctioning of the trabecular meshwork is believed to be responsible for development of glaucoma, a blinding disease. Myocilin is a gene linked to the most common form of glaucoma. Its expression is known to be upregulated by glucocorticoids in trabecular meshwork cells and the altered myocilin level may be the culprit for glaucomatous conditions such as corticosteroid-induced glaucoma. In this study, we examined the influence of myocilin overexpression on the adhesion, spreading, migration, phagocytosis, and apoptosis of human trabecular meshwork cells in culture. When the myocilin expression was increased by 3- to 4-fold, the transfectants showed a dramatic loss of actin stress fibers and focal adhesions. Cell adhesion to fibronectin and spreading were also compromised. Myocilin thus appeared to have a de-adhesive activity, similar to that reported extensively with matricellular proteins. The transfected cells in addition displayed an increased sensitivity to apoptosis. These results demonstrate that overexpression of myocilin renders trabecular meshwork cells in a de-adhesive and vulnerable state. This vulnerability may be the basis for pathologic consequences in subtypes of glaucoma.
Keywords:Myocilin   Trabecular meshwork   Transfection   Adhesion   Spreading   Migration   Phagocytosis   Apoptosis   Glaucoma   Matricellular protein
本文献已被 ScienceDirect PubMed 等数据库收录!
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号