Studies of Transforming Growth Factors Beta 1-3 and their Receptors I and II in Fibroblast of Keloids and Hypertrophic Scars

瘢痕疙瘩 增生性瘢痕 成纤维细胞 增生性瘢痕 疤痕 细胞外基质 纤维化 伤口愈合 受体 信使核糖核酸 病理 医学 人体皮肤 基因表达 生物 内科学 基因 免疫学 细胞生物学 细胞培养 生物化学 遗传学
作者
Oliver Bock,Haiyan Yu,Swantje Zitron,Ardeshir Bayat,Mark W. J. Ferguson,Ulrich Mrowietz
出处
期刊:Acta dermato-venereologica [Soc for Publication of Acta Dermato-Venereologica]
卷期号:-1 (1): 1-1 被引量:95
标识
DOI:10.1080/00015550410025453
摘要

Keloids are benign skin tumours occurring during wound healing in genetically predisposed patients. They are characterized by an abnormal deposition of extracellular matrix components, particularly collagen. There is uncertain evidence that transforming growth factor-beta (TGFss) is involved in keloid formation. Therefore we investigated the expression of TGFss1, 2 and 3 and their receptors in keloids, hypertrophic scars and normal skin. Dermal fibroblasts were obtained from punch biopsies of patients with keloids and hypertrophic scars and from normal skin of healthy individuals. Total RNA was isolated and the expression of TGFss1, 2 and 3 and of TGFss receptors I and II (TGFssRI and II) was analysed by real-time PCR using the Lightcycler technique. Our data demonstrate significantly lower TGFss2 mRNA expression in hypertrophic scar fibroblasts as compared with fibroblasts derived from keloids and normal skin (p<0.05). In contrast, TGFss3 mRNA expression was significantly lower in keloid fibroblasts in comparison with fibroblasts derived from hypertrophic scar and normal skin (p<0.01). TGFssRI mRNA expression was significantly decreased in hypertrophic scar fibroblasts (p<0.01) and TGFssRII mRNA expression was decreased in keloids compared with hypertrophic scar fibroblasts (p<0.001). The ratio of TGFssRI/TGFssRII expression was increased in keloids compared with hypertrophic scar and normal skin fibroblasts. As recently supposed, an increased TGFssRI/TGFssRII ratio could promote fibrosis. Therefore our data support a possible role of TGFssRI and TGFssRII in combination with a certain TGFss expression pattern as fibrosis-inducing factors in keloids.

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