Document Detail


Elevated tropomyosin expression is associated with epithelial-mesenchymal transition of lens epithelial cells.
MedLine Citation:
PMID:  23205574     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Eri Kubo; Nailia Hasanova; Nigar Fatma; Hiroshi Sasaki; Dhirendra P Singh
Related Documents :
12504834 - Oxidized-ldl through lox-1 increases the expression of angiotensin converting enzyme in...
24009844 - Diphlorethohydroxycarmalol, isolated from ishige okamurae, increases prostaglandin e2 t...
25059554 - Nicotine induces the production of il-1β and il-8 via the α7 nachr/nf-κb pathway in ...
23318274 - The human liver fatty acid binding protein (fabp1) gene is activated by foxa1 and ppar...
19082444 - Expression of cxcl12 and its receptor cxcr4 in esophageal squamous cell carcinoma.
16271074 - Identification of glioma-specific rfx4-e and -f isoforms and humoral immune response in...
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.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Actin Cytoskeleton / genetics,  metabolism
Actins / genetics,  metabolism
Aged
Aged, 80 and over
Animals
Capsule Opacification / genetics*,  metabolism,  pathology
Cells, Cultured
Epithelial Cells / metabolism*,  pathology
Epithelial-Mesenchymal Transition*
Female
Gene Expression
Humans
Lens Capsule, Crystalline / metabolism*,  pathology
Male
Middle Aged
Rats
Rats, Sprague-Dawley
Transfection
Tropomyosin / genetics*,  metabolism
Grant Support
ID/Acronym/Agency:
EY-13394/EY/NEI NIH HHS; EY017613/EY/NEI NIH HHS; R01 EY013394/EY/NEI NIH HHS; R01 EY017613/EY/NEI NIH HHS
Chemical
Reg. No./Substance:
0/ACTA2 protein, human; 0/Actins; 0/TPM1 protein, human; 0/TPM2 protein, human; 0/Tropomyosin
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Lichen Planopilaris After Hair Transplantation: Report of 17 Cases.
Next Document:  A re-examination of the benefits of exercise for state body satisfaction: Consideration of individua...