Latijnhouwers M A, Bergers M, Van Bergen B H, Spruijt K I, Andriessen M P, Schalkwijk J
Department of Dermatology, University Hospital Nijmegen, The Netherlands.
J Pathol. 1996 Jan;178(1):30-5. doi: 10.1002/(SICI)1096-9896(199601)178:1<30::AID-PATH442>3.0.CO;2-7.
In adult human skin, the expression of the extracellular matrix glycoprotein tenascin is limited. Under hyperproliferative conditions such as psoriasis and epidermal tumours, dermal tenascin expression is strongly upregulated. The aim of this study was to investigate the pattern and kinetics of tenascin expression in human skin during wound healing and to address the question of whether keratinocytes can directly interact with tenascin during re-epithelialization. Tenascin expression was investigated in excisional wounds in normal human skin, in explants of normal human skin, and in chronic venous ulcers, using immunohistochemistry. No tenascin staining was found directly underneath the leading edge of the sheet of migrating keratinocytes in the excisional wounds and explants. In the excisional wounds and the ulcers, dermal tenascin was strongly upregulated in areas adjacent to hyperproliferative epidermis. These hyperproliferative areas are located approximately 10-50 cells behind the leading edge, as assessed by staining for the Ki-67 antigen and the proliferating cell nuclear antigen (PCNA). At the later stages of normal wound healing and in the chronic ulcers, tenascin was also detected in the wound bed. In these areas, the dermal-epidermal junction stained positive for laminin but was negative for heparan sulphate. The absence of the latter basement membrane component suggests that the formation of a new basement membrane is not completed in these wounds. These findings suggest that tenascin is not a substrate for migrating keratinocytes; that the rapid induction of tenascin expression in the papillary dermis during wound healing results from interaction with the hyperproliferative epidermis; and that in the later stages of wound healing, keratinocytes can potentially interact with tenascin in the wound bed, because the basement membrane of the neo-epidermis is incomplete.
在成人的人类皮肤中，细胞外基质糖蛋白腱生蛋白的表达是有限的。在诸如牛皮癣和表皮肿瘤等细胞过度增殖的情况下，真皮腱生蛋白的表达会强烈上调。本研究的目的是调查伤口愈合过程中人类皮肤中腱生蛋白表达的模式和动力学，并探讨角质形成细胞在重新上皮化过程中是否能直接与腱生蛋白相互作用。使用免疫组织化学方法，对正常人类皮肤的切除伤口、正常人类皮肤外植体以及慢性静脉溃疡中的腱生蛋白表达进行了研究。在切除伤口和外植体中，迁移的角质形成细胞片层前沿正下方未发现腱生蛋白染色。在切除伤口和溃疡中，真皮腱生蛋白在与过度增殖表皮相邻的区域强烈上调。通过对Ki-67抗原和增殖细胞核抗原（PCNA）进行染色评估，这些过度增殖区域位于前沿后方约10 - 50个细胞处。在正常伤口愈合的后期以及慢性溃疡中，在伤口床也检测到了腱生蛋白。在这些区域，真皮 - 表皮连接处层粘连蛋白染色呈阳性，但硫酸乙酰肝素染色呈阴性。后者基底膜成分的缺失表明这些伤口中新基底膜的形成尚未完成。这些发现表明，腱生蛋白不是迁移角质形成细胞的底物；伤口愈合过程中乳头真皮中腱生蛋白表达的快速诱导是与过度增殖表皮相互作用的结果；并且在伤口愈合的后期，角质形成细胞可能与伤口床中的腱生蛋白相互作用，因为新表皮的基底膜不完整。
