Relationship of overexpression of angiogenesis factors and their receptors with invasive growth of keloid.
- Author:
Du-yin JIANG
1
;
Xiao-bing FU
;
Wei CHEN
;
Tong-zhu SUN
Author Information
- Publication Type:Journal Article
- MeSH: Adolescent; Adult; Aged; Angiogenesis Inducing Agents; analysis; Child; Child, Preschool; Female; Fibroblast Growth Factors; analysis; Fibroblasts; chemistry; pathology; Humans; Immunohistochemistry; Infant; Keloid; metabolism; pathology; Male; Middle Aged; Platelet-Derived Growth Factor; analysis; Receptor Protein-Tyrosine Kinases; analysis; Receptor, Fibroblast Growth Factor, Type 1; Receptor, Platelet-Derived Growth Factor alpha; analysis; Receptors, Fibroblast Growth Factor; analysis; Receptors, Growth Factor; analysis; Skin; chemistry; pathology; Vascular Endothelial Growth Factor A; analysis
- From: Chinese Journal of Plastic Surgery 2004;20(2):128-131
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the relationship between invasive growth and the angiogenesis factors and their receptors in keloid.
METHODSBiopsies from 17 keloid (Ke) were divided into atrophy group (Ke-A, n = 9), proliferating group (Ke-P, n = 13), infiltrating group (Ke-I, n = 9), normal skin around Ke (Ke-N, n = 10) and normal skin (NS, n = 10). The histology, immunohistochemistry and computerized imaging analysis were used for the study. The levels of basic fibroblast growth factor (bFGF) and its receptor-Flg, vascular endothelial growth factor (VEGF) and VEGF/KDR complex (11B5), and platelet derived growth factor (PDGF-A) and its receptor-PDGFR-alpha, and alpha-smooth muscle actin (alpha-SMA) were determined in specimens with immuneohistochemical staining.
RESULTSIn all 5 groups, bFGF, Flg, VEGF, 11B5, PDGF-A, and PDGFR-alpha were all expressed in fibroblasts (Fb), monocyte-phagocytes, vascular endothelial cells, adventitial cells, epidermal (cells and epithelial cells in appendage. The intensities of staining ranked as follows: Ke-I > Ke-N approximately equal to Ke-P > Ke-A approximately equal to NS, Flg > hFGF approximately equal to PDGFR-alpha > PDGF-A approximately equal to 11B5 > VEGF (P < 0.05 to approximately 0.01). 11B5 and VEGF were expressed (intensively in alpha-SMA positive myofibroblasts only in Ke-I group. The histological observation showed hyperplasia of endothelial cells and obliteration of microvessels.
CONCLUSIONThe invasive growth of keloid may be related to the overexpression of angiogenesis factors and their receptors. The abnormal expression of 11B5 in myofibroblasts may be one of the important factors associated with tumor-like growth feature in the invasive parts sites of keloid. The results suggest that inhibition of these biological activities would be of significance in clinical therapy.
