Jiang Du-yin, Fu Xiao-bing, Chen Wei, Sun Tong-zhu
People's Hospital of Taizhou, Taizhou 225300, China.
Zhonghua Zheng Xing Wai Ke Za Zhi. 2004 Mar;20(2):128-31.
To study the relationship between invasive growth and the angiogenesis factors and their receptors in keloid.
Biopsies 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.
In 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.
The 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.
研究瘢痕疙瘩侵袭性生长与血管生成因子及其受体之间的关系。
取自17例瘢痕疙瘩的活检标本分为萎缩组(Ke - A,n = 9)、增殖组(Ke - P,n = 13)、浸润组(Ke - I,n = 9)、瘢痕疙瘩周围正常皮肤(Ke - N,n = 10)和正常皮肤(NS,n = 10)。采用组织学、免疫组织化学及计算机图像分析进行研究。通过免疫组织化学染色测定标本中碱性成纤维细胞生长因子(bFGF)及其受体 - Flg、血管内皮生长因子(VEGF)及VEGF/KDR复合物(11B5)、血小板衍生生长因子(PDGF - A)及其受体 - PDGFR - α以及α - 平滑肌肌动蛋白(α - SMA)的水平。
在所有5组中,bFGF、Flg、VEGF、11B5、PDGF - A和PDGFR - α均在成纤维细胞(Fb)、单核吞噬细胞、血管内皮细胞、外膜细胞、表皮细胞及附属器上皮细胞中表达。染色强度排序如下:Ke - I > Ke - N≈Ke - P > Ke - A≈NS,Flg > hFGF≈PDGFR - α > PDGF - A≈11B5 > VEGF(P < 0.05至约0.01)。11B5和VEGF仅在Ke - I组的α - SMA阳性肌成纤维细胞中强烈表达。组织学观察显示内皮细胞增生和微血管闭塞。
瘢痕疙瘩的侵袭性生长可能与血管生成因子及其受体的过度表达有关。11B5在肌成纤维细胞中的异常表达可能是瘢痕疙瘩侵袭部位肿瘤样生长特征相关的重要因素之一。结果表明抑制这些生物学活性在临床治疗中具有重要意义。