Krötzsch-Gómez F E, Furuzawa-Carballeda J, Reyes-Márquez R, Quiróz-Hernández E, Díaz de León L
Department of Cellular Biology, Instituto de Investigaciones Biomédicas, UNAM, Mexico City, Mexico.
J Invest Dermatol. 1998 Nov;111(5):828-34. doi: 10.1046/j.1523-1747.1998.00329.x.
We evaluated the in situ expression of adhesion molecules (E-selectin and vascular cell-adhesion molecule) and proinflammatory/fibrogenic cytokines (IL-1beta, TNF-alpha, TGF-beta1, and PDGF) in sections of normal skin, hypertrophic scar, and hypertrophic scar previously treated with an irradiated mixture of collagen-polyvinylpyrrolidone and completely resolved. Expression of these proteins was detected by indirect immunoperoxidase staining. The hypertrophic scar group displayed an increased amount of IL-1beta, TNF-alpha, TGF-beta1, and PDGF compared with the normal skin and treated scar groups. Values were statistically significant when cytokines in hypertrophic scar and hypertrophic treated sections were compared. Surprisingly, no differences were detected between normal skin and treated scars. On the other hand, differences in levels of E-selectin and vascular cell-adhesion molecule were not statistically significant between the groups, except for vascular cell-adhesion molecule, which decreased in treated scars. Also, supernatants from fibroblast cultures derived from treated hypertrophic scar, showed a reduction in TGF-beta1 and PDGF expression, although apparently collagen synthesis was not affected. Based on previous data from clinical studies in human dermal fibrosis remodeling, and the results presented here, we suggest that collagen-polyvinylpyrrolidone modulates extracellular matrix turnover, mainly of collagen, because expression levels of IL-1beta, TNF-alpha, TGF-beta1, and PDGF were diminished. We infer that collagen-polyvinylpyrrolidone participation could also modify the inflammatory process observed in hypertrophic scarring, by diminishing the expression of adhesion molecules, as a consequence of lower levels of proinflammatory cytokines, mainly IL-1beta and TNF-alpha.
我们评估了正常皮肤、肥厚性瘢痕以及先前用胶原蛋白 - 聚乙烯吡咯烷酮辐照混合物处理并完全消退的肥厚性瘢痕切片中黏附分子(E - 选择素和血管细胞黏附分子)和促炎/纤维化细胞因子(IL - 1β、TNF - α、TGF - β1和PDGF)的原位表达。通过间接免疫过氧化物酶染色检测这些蛋白质的表达。与正常皮肤和处理后的瘢痕组相比,肥厚性瘢痕组中IL - 1β、TNF - α、TGF - β1和PDGF的含量增加。当比较肥厚性瘢痕和处理后的肥厚性瘢痕切片中的细胞因子时,差异具有统计学意义。令人惊讶的是,正常皮肤和处理后的瘢痕之间未检测到差异。另一方面,除了处理后的瘢痕中血管细胞黏附分子减少外,各组之间E - 选择素和血管细胞黏附分子水平的差异无统计学意义。此外,来自处理后的肥厚性瘢痕的成纤维细胞培养上清液显示TGF - β1和PDGF表达降低,尽管胶原蛋白合成显然未受影响。基于先前人类皮肤纤维化重塑临床研究的数据以及此处呈现的结果,我们认为胶原蛋白 - 聚乙烯吡咯烷酮可调节细胞外基质的周转,主要是胶原蛋白的周转,因为IL - 1β、TNF - α、TGF - β1和PDGF的表达水平降低。我们推断,由于促炎细胞因子(主要是IL - 1β和TNF - α)水平降低,胶原蛋白 - 聚乙烯吡咯烷酮的参与还可能通过减少黏附分子的表达来改变肥厚性瘢痕中观察到的炎症过程。