Document Detail

Elevated tropomyosin expression is associated with epithelial-mesenchymal transition of lens epithelial cells.
MedLine Citation:
PMID:  23205574     Owner:  NLM     Status:  MEDLINE    
Injury to lens epithelial cells (LECs) leads to epithelial-mesenchymal transition (EMT) with resultant fibrosis. The tropomyosin (Tpm) family of cytoskeleton proteins is involved in regulating and stabilizing actin microfilaments. Aberrant expression of Tpms leads to abnormal morphological changes with disintegration of epithelial integrity. The EMT of LECs has been proposed as a major cause of posterior capsule opacification (PCO) after cataract surgery. Using in vivo rodent PCO and human cataractous LECs, we demonstrated that the aberrant expression of rat Tpm and human Tpm1α/2β suggested their association in remodelling of the actin cytoskeleton during EMT of LECs. Expression analysis from abnormally growing LECs after lens extraction revealed elevated expression of α-smooth muscle actin (α-SMA), a marker for EMT. Importantly, these cells displayed increased expression of Tpm1α/2β following EMT/PCO formation. Expression of Tpm1α/2β was up-regulated in LECs isolated from cataractous lenses of Shumiya Cataract Rats (SCRs), compared with non-cataractous lenses. Also, LECs from human patients with nuclear cataract and anterior subcapsular fibrosis (ASF) displayed significantly increased expression of Tpm2β mRNA, suggesting that similar signalling invokes the expression of these molecules in LECs of cataractous SCR and human lenses. EMT was observed in LECs overexpressed with Tpm1α/2β, as evidenced by increased expression of α-SMA. These conditions were correlated with remodelling of actin filaments, possibly leading to EMT/PCO and ASF. The present findings may help clarify the condition of the actin cytoskeleton during morphogenetic EMT, and may contribute to development of Tpm-based inhibitors for postponing PCO and cataractogenesis.
Eri Kubo; Nailia Hasanova; Nigar Fatma; Hiroshi Sasaki; Dhirendra P Singh
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-12-04
Journal Detail:
Title:  Journal of cellular and molecular medicine     Volume:  17     ISSN:  1582-4934     ISO Abbreviation:  J. Cell. Mol. Med.     Publication Date:  2013 Jan 
Date Detail:
Created Date:  2013-01-30     Completed Date:  2013-11-13     Revised Date:  2014-01-09    
Medline Journal Info:
Nlm Unique ID:  101083777     Medline TA:  J Cell Mol Med     Country:  England    
Other Details:
Languages:  eng     Pagination:  212-21     Citation Subset:  IM    
Copyright Information:
© 2012 The Authors. Published by Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
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MeSH Terms
Actin Cytoskeleton / genetics,  metabolism
Actins / genetics,  metabolism
Aged, 80 and over
Capsule Opacification / genetics*,  metabolism,  pathology
Cells, Cultured
Epithelial Cells / metabolism*,  pathology
Epithelial-Mesenchymal Transition*
Gene Expression
Lens Capsule, Crystalline / metabolism*,  pathology
Middle Aged
Rats, Sprague-Dawley
Tropomyosin / genetics*,  metabolism
Grant Support
Reg. No./Substance:
0/ACTA2 protein, human; 0/Actins; 0/TPM1 protein, human; 0/TPM2 protein, human; 0/Tropomyosin

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