In psoriasis, nonlesional skin shows alterations at the dermal–epidermal junction compared with healthy skin. Cartilage oligomeric matrix protein (COMP) is part of the papillary dermis of healthy skin, and its expression has not yet been studied in psoriatic skin. In this study, we found that COMP localization extended deeper into the dermis and formed a more continuous layer in psoriatic nonlesional skin compared with healthy skin, whereas in psoriatic lesions, COMP showed a partially discontinuous deposition at the dermal–epidermal junction. COMP and β1-integrin showed strong colocalization in nonlesional skin, where the laminin layer within the basement membrane is discontinuous. In in vitro models, the presence of exogenous COMP decreased the proliferation rate of keratinocytes, and this proliferation-suppressing effect was diminished by blocking α5β1-integrin. Our results suggest that COMP can interact with α5β1-integrin of basal keratinocytes through the disrupted basement membrane, and this interaction might stabilize the epidermis in the nonlesional state by contributing to the suppression of keratinocyte proliferation. The antiproliferative effect of COMP is likely to be relevant to other skin diseases in which chronic nonhealing wounds are coupled with massive COMP accumulation.

在牛皮癣中，与健康皮肤相比，非病变皮肤在真皮-表皮交界处显示出变化。软骨寡聚基质蛋白（COMP）是健康皮肤的乳头状真皮的一部分，尚未在银屑病皮肤中研究其表达。在这项研究中，我们发现，与健康皮肤相比，COMP定位在牛皮癣非病变皮肤中更深地延伸至真皮，并形成了更连续的层，而在牛皮癣病变中，COMP在真皮-表皮交界处显示出部分不连续的沉积。COMP和β1-整联蛋白在非病变皮肤中表现出很强的共定位性，其中基底膜内的层粘连蛋白层是不连续的。在体外模型中，外源性COMP的存在会降低角质形成细胞的增殖速率，并且通过抑制α5β1-整联蛋白减弱了该增殖抑制作用。我们的结果表明，COMP可以通过被破坏的基底膜与基底角质形成细胞的α5β1-整联蛋白相互作用，并且这种相互作用可能通过抑制角质形成细胞的增殖而使表皮处于非损伤状态。COMP的抗增殖作用可能与其他皮肤疾病有关，在这些其他皮肤疾病中，慢性不愈合伤口伴有大量的COMP积聚。