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PMID: 2793935 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Overexpression of the vimentin gene in transgenic mice inhibits normal lens cell differentiation.

The Journal of cell biology ·Vol. 109 ·No. 4 Pt 1 ·1989-10-00 ·Pages 1653-64

Capetanaki Y, Smith S, Heath JP

Abstract

To investigate the role of the intermediate filament protein vimentin in the normal differentiation and morphogenesis of the eye lens fiber cells, we generated transgenic mice bearing multiple copies of the chicken vimentin gene. In most cases, the vimentin transgene was overexpressed in the lenses of these animals, reaching up to 10 times the endogenous levels. This high expression of vimentin interfered very strongly with the normal differentiation of the lens fibers. The normal fiber cell denucleation and elongation processes were impaired and the animals developed pronounced cataracts, followed by extensive lens degeneration. The age of appearance and extent of these abnormalities in the different transgenic lines were directly related to the vimentin level. Electron microscopic analysis revealed that the accumulated transgenic protein forms normal intermediate filaments.

MeSH Terms
Animals Blotting, Western Cataract/genetics,pathology Cell Differentiation Chickens Electrophoresis, Gel, Two-Dimensional Gene Expression Genes Lens, Crystalline/cytology,pathology,ultrastructure Mice Mice, Transgenic Microscopy, Electron Vimentin/genetics,isolation & purification,physiology
Chemicals
Vimentin
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Capetanaki Y
Department of Cell Biology, Baylor College of Medicine, Houston, Texas 77030.
Smith S
Heath J P
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Article Info
Journal
The Journal of cell biology
Abbr.
J Cell Biol
ISSN
0021-9525
DOI
10.1083/jcb.109.4.1653
Published
1989-10-00
Pages
1653-64
Language
English
Region
United States
NLM ID
0375356
PMCID
PMC2115810
Subset
IM
Grants
NIAMS NIH HHS · AR39617-01 · United States
External Links
PubMed source DOI: 10.1083/jcb.109.4.1653 PMC Full Text View journal details
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