HYALURONIC-ACID METABOLISM IN KELOID FIBROBLASTS

Citation
Sm. Alaish et al., HYALURONIC-ACID METABOLISM IN KELOID FIBROBLASTS, Journal of pediatric surgery, 30(7), 1995, pp. 949-952
Citations number
18
Categorie Soggetti
Pediatrics,Surgery
ISSN journal
00223468
Volume
30
Issue
7
Year of publication
1995
Pages
949 - 952
Database
ISI
SICI code
0022-3468(1995)30:7<949:HMIKF>2.0.ZU;2-N
Abstract
Hyaluronic acid (HA), an important component of the tissue extracellul ar matrix, is a ubiquitous glycosaminoglycan (GAG) that forms a perice llular coat on the surface of cells. It has been speculated that this pericellular HA boundary may localize cytokines, such as transforming growth factor-beta 1, which is known to stimulate collagen production. The purpose of this study was to examine the role of HA and its cell surface receptor (CD44), an active participant in HA degradation, as t hey relate to keloid formation. Dermal excisions from both normal pati ents (n = 13) and keloid patients (n = 13) were analyzed for HA conten t using an alcian blue staining technique. Fibroblast cell cultures we re used to quantitate HA synthesis and CD44 receptor density. Histolog ical analyses showed a greater HA content in keloid tissue compared wi th normal dermal tissue. In agreement with this observation, keloid fi broblasts were found to synthesize significantly more HA than normal d ermal fibroblasts (2469 +/- 483 cpm versus 1122 +/- 256 cpm, P =.02). Treatment of keloid fibroblasts with triamcinolone acetonide reduced t he level of HA synthesis to that of normal fibro blasts (1560 +/- 477 cpm versus 1293 +/- 264 cpm, P =.6). However, there was no significant difference in HA receptor density on keloid cells compared with norma l skin fibroblasts. Therefore, the increased HA deposits found in kelo ids are attributable to increased synthesis rather than to decreased d egradation mediated by the CD44 receptor. Copyright (C) 1995 by W.B. S aunders Company.