Mechanisms Underlying Trabecular Meshwork Cell Death Caused by Mutant Myocilin Expression.
10.3341/jkos.2011.52.12.1507
- Author:
Dong Hui LIM
1
;
Seongsoo SOHN
;
Tae Eun KIM
;
Changwon KEE
Author Information
1. Department of Ophthalmology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea. cw.kee@samsung.com
- Publication Type:Original Article
- Keywords:
Apoptosis;
Myocilin;
Primary open-angle glaucoma;
Trabecular meshwork
- MeSH:
Adenoviridae;
Apoptosis;
Blotting, Western;
Cell Death;
Cell Proliferation;
Cytoskeletal Proteins;
Eye Proteins;
Flow Cytometry;
Glaucoma;
Glycoproteins;
Humans;
Protein Unfolding;
Trabecular Meshwork
- From:Journal of the Korean Ophthalmological Society
2011;52(12):1507-1513
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: To determine whether the expression of mutant myocilin can lead to death of human trabecular meshwork (HTM) cells and to determine whether the mechanism by which this occurs is apoptosis. METHODS: HTM cells were transduced with a recombinant adenovirus expressing human mutant (Q368X) myocilin. The apoptotic death of HTM cells caused by expression of mutant myocilin was examined using a cell proliferation assay, flow cytometry, Western blot analysis, and immunocytochemistry. RESULTS: It appeared that the expression of mutant myocilin itself was not sufficient to cause HTM cell death. Furthermore, the expression of mutant myocilin did not lead to apoptosis of HTM cells although it did elicit a protein unfolding response. CONCLUSIONS: Our data suggest that the mechanism of myocilin glaucoma is not apoptotic death of HTM cells caused by mutant myocilin expression, and that the actual mechanism remains unknown.
