Cyr61上调人角质形成细胞系表达趋化因子与银屑病发生机制初探

Chemokines mRNA expression in HaCat induced by Cyr61 and potential relationship in pathogenesis of psoriasis

银屑病是一种常见的慢性炎症性皮肤疾病,多种炎症细胞与炎症因子参与其发病。我们已有研究发现促炎因子Cyr61/CCN1通过活化角质细胞而加剧皮损,但是否还有其他促炎机制尚不清楚。本研究通过Cyr61介导角质细胞产生趋化因子的体外实验,探讨Cyr61参与银屑病发生新途径。采用Real-time PCR方法检测人角质形成细胞系(HaCat细胞)在外源性Cyr61作用下趋化因子的表达格局。实验结果显示Cyr61能够在体外促进人角质形成细胞系表达多种趋化因子(如CCL2,CCL17,CCL22,CXCL1,CXCL10,CXCL11(P<0.05)),提示Cyr61可能通过促进角质形成细胞系表达多种趋化因子从而参与DC,Th17,Th1等细胞的趋化。提示Cyr61可能通过促进角质形成细胞系表达趋化因子介导炎性细胞局部浸润增多,加剧银屑病发病。

Psoriasis is a common chronic inflammatory skin disease, and many kinds of inflammatory cells and inflammatory factors are involved in the pathogenesis of psoriasis. Our previous studies indicate that Cyr61, a proinflammatory factor, is in- volved in the pathogenesis and development of psoriasis by promoting keratinocyte activation and proliferation resulting in ag- gravation of the skin lesions. However, whether there are other proinflammatory activity promoted by Cyr61 still remains un- clear, Therefore, in this study, we analyzed the expression profile of chemokines upon Cyr61 stimulation in vitro to explore a new pathogenesis of psoriasis. Real-time PCR was used to detect the chemokine expression pattern of HaCat cell line upon Cyr61 stimulation. Cyr61 could up-regulate the expression of multiple chemokines in HaCaT cells, such as CCL2, CCL17, CCL22, CXCL1, CXCL10,CXCL11 （P^0.05） to promote potentially DC, Th17, Thl and other cells infiltration in local skin lesions. The results indicate that Cyr61 might enhance the inflammatory cells infiltration to participate in the pathogenesis of psoriasis by inducing the expression of chemokines.