Yarosh Daniel, Dong Kelly, Smiles Kenneth
AGI Dermatics, Freeport, NY, USA.
Photochem Photobiol. 2008 Jan-Feb;84(1):67-8. doi: 10.1111/j.1751-1097.2007.00230.x.
Photoaging is a complex condition but its hallmark is the destruction of dermal collagen. This has been attributed to the direct activation of fibroblast matrix metalloproteinases by solar UV. However, we report here that unirradiated fibroblasts increase metalloproteinase production and digest collagen when exposed to cell culture media from irradiated keratinocytes. Enhanced DNA repair in the keratinocytes ameliorates this response. This suggests that soluble factors induced by DNA damage in UV-exposed epidermal keratinocytes signal collagen degradation by fibroblasts in the dermis. This motif of DNA damage in keratinocytes producing effects on other cell types mediated by soluble factors was first identified by Kripke and colleagues in studying UV-induced immune suppression.
光老化是一种复杂的状况，但其标志是真皮胶原蛋白的破坏。这被归因于太阳紫外线对成纤维细胞基质金属蛋白酶的直接激活。然而，我们在此报告，未受照射的成纤维细胞在暴露于受照射角质形成细胞的细胞培养基时会增加金属蛋白酶的产生并消化胶原蛋白。角质形成细胞中增强的DNA修复可改善这种反应。这表明紫外线暴露的表皮角质形成细胞中DNA损伤诱导的可溶性因子向真皮中的成纤维细胞发出胶原蛋白降解的信号。Kripke及其同事在研究紫外线诱导的免疫抑制时首次发现了角质形成细胞中的DNA损伤通过可溶性因子对其他细胞类型产生影响的这一模式。
