Mechanisms Underlying Trabecular Meshwork Cell Death Caused by Mutant Myocilin Expression. |
Dong Hui Lim, Seongsoo Sohn, Tae Eun Kim, Changwon Kee |
1Department of Ophthalmology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea. cw.kee@samsung.com 2Center for Clinical Research, Samsung Biomedical Research Institute, Seoul, Korea. |
돌연변이 마이오실린 발현에 의한 섬유주세포 사멸 및 그 기전 |
임동희1⋅손성수1⋅김태은2⋅기창원1 |
Department of Ophthalmology, Samsung Medical Center, Sungkyunkwan University School of Medicine1, Seoul, Korea Center for Clinical Research, Samsung Biomedical Research Institute2, Seoul, Korea |
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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. |
Key Words:
Apoptosis;Myocilin;Primary open-angle glaucoma;Trabecular meshwork |
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