阿维A通过依赖STAT1和STAT3的信号传导调节HaCaT细胞增殖。
Acitretin modulates HaCaT cells proliferation through STAT1- and STAT3-dependent signaling.
作者信息
Qin Xuan, Chen Chunna, Zhang Yuan, Zhang Li, Mei Yijie, Long Xinchun, Tan Rui, Liang Wenli, Sun Ledong
机构信息
Department of Dermatology, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China.
Department of Dermatology, The First People's Hospital of Chenzhou, Chenzhou 423000, China.
出版信息
Saudi Pharm J. 2017 May;25(4):620-624. doi: 10.1016/j.jsps.2017.04.034. Epub 2017 May 8.
Acitretin has been a valuable option for the treatment of psoriasis, however, the molecular events of acitretin leading to the normalization of keratinocytes differentiation on psoriasis patients have not been fully explored. To investigate whether there were certain relationship between keratinocytes proliferation and JAK/STAT signaling pathways in psoriasis, and how acitretin modulated the signaling pathways. HaCaT cells, an in vitro immortal human keratinocyte cell line, was chosen as a in vitro model of psoriasis. The small interfering RNA targeting STAT1 (siRNA-STAT1) and STAT3 (siRNA-STAT3) were subsequently transfected into the HaCaT cells which were treated with or without acitretin. We found that HaCaT cells proliferation and the expression of STAT1 or STAT3 were inhibited by acitretin, siRNA-STAT1 and siRNA-STAT3. Our experimental data shows that acitretin might inhibit HaCaT cells proliferation in psoriasis by decreasing the expression of STAT- and STAT3-dependent mechanism.
阿维A一直是治疗银屑病的一个有价值的选择，然而，阿维A导致银屑病患者角质形成细胞分化正常化的分子机制尚未完全阐明。为了研究银屑病中角质形成细胞增殖与JAK/STAT信号通路之间是否存在特定关系，以及阿维A如何调节该信号通路。选择体外永生化的人角质形成细胞系HaCaT细胞作为银屑病的体外模型。随后将靶向STAT1（siRNA-STAT1）和STAT3（siRNA-STAT3）的小干扰RNA转染到用或不用阿维A处理的HaCaT细胞中。我们发现阿维A、siRNA-STAT1和siRNA-STAT3均可抑制HaCaT细胞增殖以及STAT1或STAT3的表达。我们的实验数据表明，阿维A可能通过降低STAT1和STAT3依赖性机制的表达来抑制银屑病中HaCaT细胞的增殖。
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