Zhang L Q, Laato M, Muona P, Penttinen R, Oikarinen A, Peltonen J
Department of Medical Biochemistry, University of Turku, Finland.
Arch Dermatol Res. 1995;287(6):534-8. doi: 10.1007/BF00374072.
The present study was designed to investigate the expression of type I, III and VI collagens by a fibroblast cell line initiated from a hypertrophic scar. The same tissue has previously been demonstrated to display markedly elevated expression of type I and III collagen mRNAs in vivo. Unexpectedly, slot-blot and Northern hybridizations revealed a barely detectable steady-state level of pro alpha 1(III) collagen chain mRNA in cultured hypertrophic scar fibroblasts. The levels of pro alpha 1(I) and alpha 2(VI) collagen chain mRNAs were essentially the same in fibroblasts cultured from hypertrophic scar and in fibroblasts cultured from normal skin. However, Northern blot analyses indicated that the ratio of 5.8 kb to 4.8 kb species of pro alpha 1(I) collagen mRNA was slightly reduced in fibroblasts originating from the hypertrophic scar compared to that in normal fibroblasts. When normal fibroblasts were incubated in conditioned medium from hypertrophic scar cultures, the expression of pro alpha 1(III) collagen chain mRNA decreased to a markedly lower level. Our studies suggest that collagen synthesis by fibroblasts in hypertrophic scars is stimulated by humoral factors which are active only in vivo. Furthermore, the results suggest that fibroblasts cultured from hypertrophic scar display a selective downregulation of different collagen genes and that this downregulation is exerted through an autocrine mechanism.
本研究旨在调查源自增生性瘢痕的成纤维细胞系中I型、III型和VI型胶原蛋白的表达情况。先前已证明同一组织在体内I型和III型胶原蛋白mRNA的表达显著升高。出乎意料的是,狭缝印迹和Northern杂交显示,在培养的增生性瘢痕成纤维细胞中,前α1(III)胶原蛋白链mRNA的稳态水平几乎检测不到。增生性瘢痕培养的成纤维细胞和正常皮肤培养的成纤维细胞中,前α1(I)和α2(VI)胶原蛋白链mRNA的水平基本相同。然而,Northern印迹分析表明,与正常成纤维细胞相比,源自增生性瘢痕的成纤维细胞中,5.8 kb与4.8 kb的前α1(I)胶原蛋白mRNA种类的比例略有降低。当正常成纤维细胞在增生性瘢痕培养物的条件培养基中孵育时,前α1(III)胶原蛋白链mRNA的表达下降到明显更低的水平。我们的研究表明,增生性瘢痕中成纤维细胞的胶原蛋白合成受到仅在体内具有活性的体液因子的刺激。此外,结果表明,源自增生性瘢痕的培养成纤维细胞表现出不同胶原蛋白基因的选择性下调,并且这种下调是通过自分泌机制实现的。