Hyaluronic acid metabolism in keloid fibroblasts

Samuel M. Alaish, Dorne R. Yager, Robert F. Diegelmann, I. Kelman Cohen

Research output: Contribution to journalArticle

Abstract

Hyaluronic acid (HA), an important component of the tissue extracellular matrix, is a ubiquitous glycosaminoglycan (GAG) that forms a pericellular coat on the surface of cells. It has been speculated that this pericellular HA boundary may localize cytokines, such as transforming growth factor-β1, 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 they relate to keloid formation. Dermal excisions from both normal patients (n = 13) and keloid patients (n = 13) were analyzed for HA content using an alcian blue staining technique. Fibroblast cell cultures were used to quantitate HA synthesis and CD44 receptor density. Histological analyses showed a greater HA content in keloid tissue compared with normal dermal tissue. In agreement with this observation, keloid fibroblasts were found to synthesize significantly more HA than normal dermal fibroblasts (2469 ± 483 cpm versus 1122 ± 256 cpm, P = .02). Treatment of keloid fibroblasts with triamcinolone acetonide reduced the level of HA synthesis to that of normal fibroblasts (1560 ± 477 cpm versus 1293 ± 264 cpm, P = .6). However, there was no significant difference in HA receptor density on keloid cells compared with normal skin fibroblasts. Therefore, the increased HA deposits found in keloids are attributable to increased synthesis rather than to decreased degradation mediated by the CD44 receptor.

Original languageEnglish (US)
Pages (from-to)949-952
Number of pages4
JournalJournal of Pediatric Surgery
Volume30
Issue number7
DOIs
StatePublished - 1995
Externally publishedYes

Fingerprint

Keloid
Hyaluronic Acid
Fibroblasts
Skin
Triamcinolone Acetonide
Alcian Blue
Cell Surface Receptors
Transforming Growth Factors
Glycosaminoglycans
Extracellular Matrix
Collagen
Cell Culture Techniques

Keywords

  • CD44 receptor
  • fibroblast
  • Hyaluronic acid
  • keloid
  • triamcinolone
  • wound healing

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Surgery

Cite this

Hyaluronic acid metabolism in keloid fibroblasts. / Alaish, Samuel M.; Yager, Dorne R.; Diegelmann, Robert F.; Cohen, I. Kelman.

In: Journal of Pediatric Surgery, Vol. 30, No. 7, 1995, p. 949-952.

Research output: Contribution to journalArticle

Alaish, Samuel M. ; Yager, Dorne R. ; Diegelmann, Robert F. ; Cohen, I. Kelman. / Hyaluronic acid metabolism in keloid fibroblasts. In: Journal of Pediatric Surgery. 1995 ; Vol. 30, No. 7. pp. 949-952.
@article{9ed13a1055be41819e60fa0d86ea3a4c,
title = "Hyaluronic acid metabolism in keloid fibroblasts",
abstract = "Hyaluronic acid (HA), an important component of the tissue extracellular matrix, is a ubiquitous glycosaminoglycan (GAG) that forms a pericellular coat on the surface of cells. It has been speculated that this pericellular HA boundary may localize cytokines, such as transforming growth factor-β1, 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 they relate to keloid formation. Dermal excisions from both normal patients (n = 13) and keloid patients (n = 13) were analyzed for HA content using an alcian blue staining technique. Fibroblast cell cultures were used to quantitate HA synthesis and CD44 receptor density. Histological analyses showed a greater HA content in keloid tissue compared with normal dermal tissue. In agreement with this observation, keloid fibroblasts were found to synthesize significantly more HA than normal dermal fibroblasts (2469 ± 483 cpm versus 1122 ± 256 cpm, P = .02). Treatment of keloid fibroblasts with triamcinolone acetonide reduced the level of HA synthesis to that of normal fibroblasts (1560 ± 477 cpm versus 1293 ± 264 cpm, P = .6). However, there was no significant difference in HA receptor density on keloid cells compared with normal skin fibroblasts. Therefore, the increased HA deposits found in keloids are attributable to increased synthesis rather than to decreased degradation mediated by the CD44 receptor.",
keywords = "CD44 receptor, fibroblast, Hyaluronic acid, keloid, triamcinolone, wound healing",
author = "Alaish, {Samuel M.} and Yager, {Dorne R.} and Diegelmann, {Robert F.} and Cohen, {I. Kelman}",
year = "1995",
doi = "10.1016/0022-3468(95)90319-4",
language = "English (US)",
volume = "30",
pages = "949--952",
journal = "Journal of Pediatric Surgery",
issn = "0022-3468",
publisher = "W.B. Saunders Ltd",
number = "7",

}

TY - JOUR

T1 - Hyaluronic acid metabolism in keloid fibroblasts

AU - Alaish, Samuel M.

AU - Yager, Dorne R.

AU - Diegelmann, Robert F.

AU - Cohen, I. Kelman

PY - 1995

Y1 - 1995

N2 - Hyaluronic acid (HA), an important component of the tissue extracellular matrix, is a ubiquitous glycosaminoglycan (GAG) that forms a pericellular coat on the surface of cells. It has been speculated that this pericellular HA boundary may localize cytokines, such as transforming growth factor-β1, 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 they relate to keloid formation. Dermal excisions from both normal patients (n = 13) and keloid patients (n = 13) were analyzed for HA content using an alcian blue staining technique. Fibroblast cell cultures were used to quantitate HA synthesis and CD44 receptor density. Histological analyses showed a greater HA content in keloid tissue compared with normal dermal tissue. In agreement with this observation, keloid fibroblasts were found to synthesize significantly more HA than normal dermal fibroblasts (2469 ± 483 cpm versus 1122 ± 256 cpm, P = .02). Treatment of keloid fibroblasts with triamcinolone acetonide reduced the level of HA synthesis to that of normal fibroblasts (1560 ± 477 cpm versus 1293 ± 264 cpm, P = .6). However, there was no significant difference in HA receptor density on keloid cells compared with normal skin fibroblasts. Therefore, the increased HA deposits found in keloids are attributable to increased synthesis rather than to decreased degradation mediated by the CD44 receptor.

AB - Hyaluronic acid (HA), an important component of the tissue extracellular matrix, is a ubiquitous glycosaminoglycan (GAG) that forms a pericellular coat on the surface of cells. It has been speculated that this pericellular HA boundary may localize cytokines, such as transforming growth factor-β1, 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 they relate to keloid formation. Dermal excisions from both normal patients (n = 13) and keloid patients (n = 13) were analyzed for HA content using an alcian blue staining technique. Fibroblast cell cultures were used to quantitate HA synthesis and CD44 receptor density. Histological analyses showed a greater HA content in keloid tissue compared with normal dermal tissue. In agreement with this observation, keloid fibroblasts were found to synthesize significantly more HA than normal dermal fibroblasts (2469 ± 483 cpm versus 1122 ± 256 cpm, P = .02). Treatment of keloid fibroblasts with triamcinolone acetonide reduced the level of HA synthesis to that of normal fibroblasts (1560 ± 477 cpm versus 1293 ± 264 cpm, P = .6). However, there was no significant difference in HA receptor density on keloid cells compared with normal skin fibroblasts. Therefore, the increased HA deposits found in keloids are attributable to increased synthesis rather than to decreased degradation mediated by the CD44 receptor.

KW - CD44 receptor

KW - fibroblast

KW - Hyaluronic acid

KW - keloid

KW - triamcinolone

KW - wound healing

UR - http://www.scopus.com/inward/record.url?scp=0029120878&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029120878&partnerID=8YFLogxK

U2 - 10.1016/0022-3468(95)90319-4

DO - 10.1016/0022-3468(95)90319-4

M3 - Article

C2 - 7472951

AN - SCOPUS:0029120878

VL - 30

SP - 949

EP - 952

JO - Journal of Pediatric Surgery

JF - Journal of Pediatric Surgery

SN - 0022-3468

IS - 7

ER -