Co-expression of colligin and collagen in oral submucous fibrosis: plausible role in pathogenesis

Citation
J. Kaur et al., Co-expression of colligin and collagen in oral submucous fibrosis: plausible role in pathogenesis, ORAL ONCOL, 37(3), 2001, pp. 282-287
Citations number
30
Categorie Soggetti
Oncology
Journal title
ORAL ONCOLOGY
ISSN journal
13688375 → ACNP
Volume
37
Issue
3
Year of publication
2001
Pages
282 - 287
Database
ISI
SICI code
1368-8375(200104)37:3<282:COCACI>2.0.ZU;2-S
Abstract
The high incidence of oral submucous fibrosis (OSF), a potentially malignan t condition of the oral cavity, in the Indian subcontinent is causally asso ciated with commonly prevailing habit of chewing areca nut and tobacco. Kno wledge of molecular alterations in OSF is meagre. OSF is characterised by p rogressive accumulation of collagen fibres in lamina propria and oral submu cosa. Colligin/HSP47 is a 47KDa stress protein which acts as a chaperone fo r collagen. We hypothesized that since colligin plays a vital role in foldi ng and assembling collagen it may be involved in the pathogenesis of OSF. T he present study was undertaken in tobacco and areca nut chewing Indian OSF patients to investigate the correlation, if any, between the expression of colligin and collagen type I proteins in OSF lesions. Immunohistochemical analysis showed overexpression of colligin and collagen type I proteins in 16/23 (70%) and 15/23 (65%) of OSF cases, respectively. The hallmark of the study was the significant association between the increased expression of type I collagen and its chaperone, colligin, in OSF lesions (P = 0.0494). T he data suggest that the increased levels of colligin in OSF may contribute to the deposition of collagen and consequent increased fibrosis in the ora l submucosa in OSF lesions. (C) 2001 Elsevier Science Ltd. All rights reser ved.