Atopic dermatitis (AD) is a relapsing inflammatory skin disease with a complicated pathogenesis. This study aimed to investigate whether miR-375-3p could regulate AD through the Yes-associated protein 1 (YAP1) pathway. In this study, inflammatory response was induced by TNF-α and IFN-γ administration in HaCaT cells. We found that viability and inflammatory factor release, including interleukin-1β (IL-1β) and IL-6, were negatively related to miR-375-3p expression in HaCaT cells. We also found that YAP1 overexpression down-regulated lympho-epithelial Kazal type inhibitor (LEKTI) levels and aggravated viability and inflammation in TNF-α and IFN-γ-treated HaCaT cells. Dual-luciferase reporter assay proved the targeted binding of miR-375-3p and YAP1 3ʹ-UTR. Additionally, the protective effect of miR-375-3p on inflammatory response in TNF-α and IFN-γ-treated HaCaT cells could be impeded by YAP1 overexpression. Collectively, our results suggested that miR-375-3p could modulate HaCaT cell viability and inflammation through the YAP1/LEKTI pathway.

特应性皮炎（AD）是一种复发性炎症性皮肤病，发病机理复杂。这项研究旨在调查miR-375-3p是否可以通过Yes相关蛋白1（YAP1）途径调节AD。在这项研究中，通过在HaCaT细胞中给予TNF-α和IFN-γ诱导炎症反应。我们发现活力和炎性因子释放，包括白介素-1β（IL-1β）和IL-6，与HaCaT细胞中miR-375-3p表达负相关。我们还发现，在TNF-α和IFN-γ处理的HaCaT细胞中，YAP1过表达下调了淋巴上皮Kazal型抑制剂（LEKTI）的水平，并加剧了生存能力和炎症。双荧光素酶报告基因检测证明了miR-375-3p和YAP1 3′-UTR的靶向结合。另外，YAP1过表达可能会阻碍miR-375-3p对TNF-α和IFN-γ处理的HaCaT细胞炎症反应的保护作用。总体而言，我们的结果表明，miR-375-3p可以通过YAP1 / LEKTI途径调节HaCaT细胞的活力和炎症。