Oono T, Specks U, Eckes B, Majewski S, Hunzelmann N, Timpl R, Krieg T
Department of Dermatology, University of Cologne, Köln, Germany.
J Invest Dermatol. 1993 Mar;100(3):329-34. doi: 10.1111/1523-1747.ep12470022.
During the highly regulated process of wound healing the expression of the interstitial collagens I and III is increased in a time-dependent fashion. Although ultrastructural and in vitro studies suggest a physiologic role of collagen VI in the organization of extracellular matrix deposition, nothing is known about its role in wound healing. Therefore, we studied collagen VI gene expression during wound healing in humans compared to that of collagens I and III. The presence of specific alpha 1(VI) and alpha 3(VI) mRNA species in scar tissue was demonstrated by Northern blot analysis. Quantification of mRNA expression by dot blot analysis and in situ hybridization indicated that like for the interstitial collagens I and III collagen VI gene expression was increased during wound healing, reaching its maximum 2 weeks after initial insult. In the late phase of wound healing like alpha 1(I) the alpha 1(VI) gene expression was not down regulated significantly. In contrast, a reduction of alpha 3(VI) collagen gene expression was observed, as was for the alpha 1(III) collagen gene, indicating a non-coordinate regulation of these chains. Collagen VI gene expression could be localized to fibroblast-like cells and to endothelial cells of newly formed vessels. Collagen VI gene expression was undetectable in smooth muscle cells and myoepithelial cells of eccrine glands. These results indicate that collagen VI gene expression is regulated in a time-dependent fashion and that fibroblasts and endothelial cells appear to play an important role in collagen VI synthesis during wound healing.
在高度受控的伤口愈合过程中,I型和III型间质胶原的表达呈时间依赖性增加。尽管超微结构和体外研究表明VI型胶原在细胞外基质沉积的组织过程中具有生理作用,但其在伤口愈合中的作用尚不清楚。因此,我们研究了人类伤口愈合过程中VI型胶原基因的表达,并与I型和III型胶原进行了比较。通过Northern印迹分析证实了瘢痕组织中存在特异性的α1(VI)和α3(VI)mRNA。通过斑点印迹分析和原位杂交对mRNA表达进行定量分析表明,与I型和III型间质胶原一样,VI型胶原基因表达在伤口愈合过程中增加,在初始损伤后2周达到最大值。在伤口愈合后期,与α1(I)一样,α1(VI)基因表达没有明显下调。相反,观察到α3(VI)胶原基因表达减少,α1(III)胶原基因也是如此,这表明这些链的调节不协调。VI型胶原基因表达可定位于成纤维细胞样细胞和新形成血管的内皮细胞。在小汗腺的平滑肌细胞和肌上皮细胞中未检测到VI型胶原基因表达。这些结果表明,VI型胶原基因表达受时间依赖性调节,成纤维细胞和内皮细胞在伤口愈合过程中VI型胶原合成中似乎起重要作用。