Chaquour B, Seité S, Coutant K, Fourtanier A, Borel J P, Bellon G
Laboratoire de Biochimie, Faculté de Médecine, CNRS ERS F0017, Reims, France.
J Photochem Photobiol B. 1995 May;28(2):125-35. doi: 10.1016/1011-1344(94)07080-8.
Histochemical and ultrastructural studies have already demonstrated that chronic exposure to UV radiation induces profound alterations in all structural elements of the skin and that topical all-trans retinoic acid (tRA) can substantially correct much of the tissue damage. However, previous biochemical studies on dermal components of the extracellular matrix have led to contradictory results, particularly with regard to the effect of chronic UV exposure. The aim of our study was to investigate changes in collagen content and other dermal modifications induced by tRA in irradiated and non-irradiated hairless mouse skin. Hairless mice were exposed to increasing doses of UVB for 10 weeks (the cumulative total dose was 4.6 J cm-2). After the UV irradiation period the animals were treated with 0.05% tRA or with ethanol-polyethylene glycol vehicle alone three times a week for up to 10 weeks. Non-irradiated animals underwent the same treatments. The main clinical and histological changes induced by UVB exposure were erythema, wrinkling, keratosis and epidermal thickening. Following UVB exposure, tRA treatment did not improve the clinical aspect but increased the width of the dermal repair zone. Fibronectin, laminin and type I and VI collagens were detected by indirect immunofluorescence techniques in this zone. Type I and III collagens were quantitated in skin fragments after cyanogen bromide digestion and polyacrylamide gel electrophoresis. Under our experimental conditions, UVB irradiation alone induced neither changes in total collagen nor in type I and III collagen levels. tRA treatment of irradiated skin significantly increased both type I and III collagen levels by factors of 1.33 and 1.88 respectively. The ratio of type III to types I + III increased significantly. Topical tRA also increased collagen type levels in non-irradiated hairless mouse skin. Type I collagen increased proportionally to type III. This study leads to the conclusion that topical tRA exerts direct or indirect effects on collagen metabolism in irradiated as well as non-irradiated hairless mouse skin.
组织化学和超微结构研究已经表明，长期暴露于紫外线辐射会导致皮肤所有结构成分发生深刻变化，而局部外用全反式维甲酸（tRA）能够在很大程度上纠正大部分组织损伤。然而，先前关于细胞外基质真皮成分的生化研究得出了相互矛盾的结果，尤其是在长期紫外线暴露的影响方面。我们研究的目的是调查tRA在照射和未照射的无毛小鼠皮肤中引起的胶原蛋白含量变化及其他真皮改变。将无毛小鼠暴露于递增剂量的UVB下10周（累积总剂量为4.6 J/cm²）。在紫外线照射期后，动物每周接受3次0.05% tRA或仅用乙醇 - 聚乙二醇载体处理，持续长达10周。未照射的动物接受相同的处理。UVB暴露引起的主要临床和组织学变化为红斑、皱纹、角化病和表皮增厚。UVB暴露后，tRA治疗并未改善临床症状，但增加了真皮修复区的宽度。通过间接免疫荧光技术在该区域检测到纤连蛋白、层粘连蛋白以及I型和VI型胶原蛋白。在溴化氰消化和聚丙烯酰胺凝胶电泳后，对皮肤碎片中的I型和III型胶原蛋白进行定量。在我们的实验条件下，单独的UVB照射既未引起总胶原蛋白变化，也未引起I型和III型胶原蛋白水平变化。tRA处理照射后的皮肤显著增加了I型和III型胶原蛋白水平，分别增加了1.33倍和1.88倍。III型与I型 + III型的比例显著增加。局部tRA也增加了未照射的无毛小鼠皮肤中的胶原蛋白类型水平。I型胶原蛋白与III型胶原蛋白成比例增加。本研究得出结论，局部tRA对照射和未照射的无毛小鼠皮肤中的胶原蛋白代谢具有直接或间接影响。
