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Invest Ophthalmol Vis Sci 2007;48: E-Abstract 5864.
© 2007 ARVO

5864—B546

Lysosomal Traffic and Degradation of ßig-h3 Protein

E.-K. Kim1,2, H.-J. Cho1, S.-Y. Ahn1, Y.-J. Choi1,2, T.-I. Kim1, S. Cristol3 and S.-I. Choi1

1Corneal Dystrophy Research Institute & Department of Ophthalmology, Yonsei Univ College of Med, Seoul, Republic of Korea
2Team of Nanobiomaterials for Cell-Based Implants, Yonsei University, Seoul, Republic of Korea
3Emory Eye Center, Emory Univ, Atlanta, Georgia

Commerical Relationships: E. Kim, None; H. Cho, None; S. Ahn, None; Y. Choi, None; T. Kim, None; S. Cristol, None; S. Choi, None.

Support: Supported by a grant of the Korea Health 21 R&D Project, Ministry of Health & Welfare, Republic of Korea (grant no.: 02-PJ1-PG1-CH02-0003).

Abstract

Purpose:To investigate intracellular traffic and degradation of ßig-h3 protein, a protein associated with amyloid deposition in granular corneal dystrophy Type II (GCDII).

Methods:Corneal fibroblasts were treated with proteasomal inhibitors, lactacystin and MG132, or lysosomal inhibitors, bafilomycin A1 for 12 h. We used immunoblot analysis to measure ßig-h3 protein in cell lysate.

Results:The lysosomal inhibitors, bafilomycin A1, significantly blocked ßig-h3 protein degradation in a dose-dependent manner in cultured corneal fibroblasts. In contrast, proteasomal inhibitor, MG132, did not lead to significant accumulation of ßig-h3 protein. The internalization of ßig-h3 is inhibited by nystatin, which blocks lipid raft endocytosis, but not by chlorpromazine which is known to block clathrin-mediated endocytosis. Moreover, ßig-h3 endocytosis was decreased significantly in TGF-ß1-exposed cultured corneal fibroblasts.

Conclusions:These results demonstrate that ßig-h3 protein degradation is mediated by an autophagy/lysosomes pathway. Alterations both in lysosomal degradation and in expression of ßig-h3 induced by TGF-ß1 may contribute to amyloid deposition of ßig-h3 in GCDII.

Key Words: cornea: basic science • degenerations/dystrophies • cornea: stroma and keratocytes

© 2007, The Association for Research in Vision and Ophthalmology, Inc., all rights reserved. Permission to republish any abstract or part of an abstract in any form must be obtained in writing from the ARVO Office prior to publication.




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