Keratinocyte-derived growth factors play a role in the formation of hypertrophic scars

被引:127
作者
Niessen, FB
Andriessen, MP
Schalkwijk, J
Visser, L
Timens, W
机构
[1] Univ Groningen Hosp, Dept Plast Reconstruct & Hand Surg, NL-9700 RB Groningen, Netherlands
[2] Univ Nijmegen Hosp, Dept Dermatol, Nijmegen, Netherlands
[3] Univ Groningen Hosp, Dept Pathol, Groningen, Netherlands
关键词
skin; epidermis; hypertrophic scar; keratinocyte; growth factor;
D O I
10.1002/path.853
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
In predisposed individuals, wound healing can lead to hypertrophic scar or keloid formation, characterized by an overabundant extracellular matrix. It has recently been shown that hypertrophic scars are accompanied by abnormal keratinocyte differentiation and proliferation, and significantly increased acanthosis, compared with normal scars. This study addressed the question of whether the development of normal and hypertrophic scars is regulated by differences in the growth factor profiles of both the epidermis and the dermis, The presence of interleukin-l alpha (IL-1 alpha), IL-1 beta, tumour necrosis factor-alpha (TNF-alpha), platelet-derived growth factor (PDGF), transforming growth factor-beta1 (TGF-beta1), and basic fibroblast growth factor (bFGF) was investigated in biopsies taken from breast reduction scars at 3 and 12 months following surgery. The samples were analysed by immunohistological methods and categorized as scars that remained hypertrophic (HH), became normal (HN) or remained normal after 12 months (NN), The epidermal expression of IL-1 alpha was significantly increased in NN scars compared with HN and HH scars 3 and 12 months following operation, whereas the dermal expression showed no difference. PDGF was significantly increased in the dermis of normal scars after 3 months and in both the epidermis and the dermis of hypertrophic scars after 12 months. IL-1 beta, TNF-alpha, TGF-beta and bFGF showed no differences. It is hypothesized that impaired production of keratinocytederived growth factors, such as IL-1 alpha, leads to a decrease in the catabolism of the dermal matrix, whereas augmented epidermal PDGF production leads to increased formation of the dermal matrix in hypertrophic scars. These observations support the possibility that the epidermis is involved in preventing the formation of hypertrophic scars, Copyright (C) 2001 John Wiley & Sons, Ltd.
引用
收藏
页码:207 / 216
页数:10
相关论文
共 81 条
[1]   BIOCHEMICAL-COMPOSITION OF THE CONNECTIVE-TISSUE IN KELOIDS AND ANALYSIS OF COLLAGEN-METABOLISM IN KELOID FIBROBLAST-CULTURES [J].
ABERGEL, RP ;
PIZZURRO, D ;
MEEKER, CA ;
LASK, G ;
MATSUOKA, LY ;
MINOR, RR ;
CHU, ML ;
UITTO, J .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1985, 84 (05) :384-390
[2]  
Adriessen MP, 1998, J PATHOL, V186, P192, DOI 10.1002/(SICI)1096-9896(1998100)186:2<192::AID-PATH163>3.0.CO
[3]  
2-X
[4]   HUMAN KERATINOCYTES ARE A MAJOR SOURCE OF CUTANEOUS PLATELET-DERIVED GROWTH-FACTOR [J].
ANSEL, JC ;
TIESMAN, JP ;
OLERUD, JE ;
KRUEGER, JG ;
KRANE, JF ;
TARA, DC ;
SHIPLEY, GD ;
GILBERTSON, D ;
USUI, ML ;
HART, CE .
JOURNAL OF CLINICAL INVESTIGATION, 1993, 92 (02) :671-678
[5]   FIBRONECTIN IS OVERPRODUCED BY KELOID FIBROBLASTS DURING ABNORMAL WOUND-HEALING [J].
BABU, M ;
DIEGELMANN, R ;
OLIVER, N .
MOLECULAR AND CELLULAR BIOLOGY, 1989, 9 (04) :1642-1650
[6]  
BASSOLS A, 1988, J BIOL CHEM, V263, P3039
[7]   Upregulation of cell-surface-associated plasminogen activation in cultured keratinocytes by interleukin-1 beta and tumor necrosis factor-alpha [J].
Bechtel, MJ ;
Reinartz, J ;
Rox, JM ;
Inndorf, S ;
Schaefer, BM ;
Kramer, MD .
EXPERIMENTAL CELL RESEARCH, 1996, 223 (02) :395-404
[8]   GROWTH-FACTORS AND WOUND-HEALING - BIOCHEMICAL-PROPERTIES OF GROWTH-FACTORS AND THEIR RECEPTORS [J].
BENNETT, NT ;
SCHULTZ, GS .
AMERICAN JOURNAL OF SURGERY, 1993, 165 (06) :728-737
[9]   GROWTH-FACTORS AND WOUND-HEALING .2. ROLE IN NORMAL AND CHRONIC WOUND-HEALING [J].
BENNETT, NT ;
SCHULTZ, GS .
AMERICAN JOURNAL OF SURGERY, 1993, 166 (01) :74-81
[10]   KELOIDS [J].
BERMAN, B ;
BIELEY, HC .
JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY, 1995, 33 (01) :117-123