miR-20a靶向STAT3抑制角质形成细胞增殖参与银屑病的机制

Mechanism of miR-20a Targeting STAT3 Inhibiting Keratinocyte Proliferation and Participating in Psoriasis

目的探讨miR-20a是否可靶向调控STAT3表达影响角质形成细胞增殖参与银屑病发生发展过程。方法QPCR检测银屑病患者正常皮肤和皮损组织中miR-20a、STAT3的表达情况,统计分析二者间的表达相关性;QPCR检测miR-20a表达变化对STAT3水平的影响;LUC验证miR-20a和STAT3间的靶向关系;miRNA mimics和STAT3过表达载体共转染后,MTT检测HaCaT细胞的增殖活性。结果miR-20a在银屑病患者皮损组织中特异性低表达,STAT3在皮损组织中高表达,且miR-20a与STAT3表达呈负相关性;QPCR检测miR-20a表达变化对STAT3的影响后发现miR-20a可抑制STAT3表达;LUC实验发现miR-20a可靶向结合STAT3;MTT功能实验结果表明STAT3过表达可增强角质形成细胞增殖活性,而过表达miR-20a不仅可抑制细胞增殖活性和STAT3的表达,还可部分逆转STAT3对细胞增殖的促进作用。结论miR-20a可靶向STAT3抑制角质形成细胞过度增殖,在银屑病发生发展中发挥保护作用。

Objective To explore the role and mechanism of miR-20 a in psoriasis lesions and HaCaT cells. Methods QPCR was used to detect the expression of miR-20 a and STAT3 in normal skin and psoriasis lesions, QPCR was used to detect the effect of miR-20 a expression on STAT3 level in HaCaT cells,LUC verified the relationship between miR-20 a and STAT3.After co-transfection of miRNA mimics and STAT3 overexpression vectors,MTT assayed the proliferative of HaCaT cells.Results miR-20 a was lower expressed in the lesions′ and STAT3 was highly expressed.miR-20 a was negatively correlated with STAT3 expression.miR-20 a can inhibit STAT3 expression in HaCaT cells,STAT3 over expression can enhance the proliferation of keratinocytes,while overexpression of miR-20 a can inhibit cell proliferation. Conclusion miR-20 a can target STAT3 to inhibit hyperproliferation of keratinocytes and play a protective role in the pathogenesisof psoriasis.