Open AccessElevated tropomyosin expression is associated with epithelial–mesenchymal transition of lens epithelial cells
Author(s) -
Kubo Eri,
Hasanova Nailia,
Fatma Nigar,
Sasaki Hiroshi,
Singh Dhirendra P.
Publication year - 2013
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/j.1582-4934.2012.01654.x
Subject(s) - cytoskeleton , epithelial–mesenchymal transition , actin , microbiology and biotechnology , tropomyosin , biology , fibrosis , actin cytoskeleton , chemistry , pathology , downregulation and upregulation , cell , biochemistry , gene , medicine
Injury to lens epithelial cells ( LEC s) 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 LEC s has been proposed as a major cause of posterior capsule opacification ( PCO ) after cataract surgery. Using in vivo rodent PCO and human cataractous LEC s, 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 LEC s. Expression analysis from abnormally growing LEC s 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 LEC s isolated from cataractous lenses of Shumiya Cataract Rats ( SCR s), compared with non‐cataractous lenses. Also, LEC s from human patients with nuclear cataract and anterior subcapsular fibrosis ( ASF ) displayed significantly increased expression of Tpm2β m RNA , suggesting that similar signalling invokes the expression of these molecules in LEC s of cataractous SCR and human lenses. EMT was observed in LEC s 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.