Deletion of NFIA Leads to Activation of S100A7 and Inflammatory Response-Induced Apoptosis of Keratinocytes in Oral Lichen Planus Progression.

S100 calcium-binding protein A7 (S100A7) has been implicated in psoriasis and other inflammatory diseases. However, the function of S100A7 in oral lichen planus (OLP), a chronic inflammatory disease, remains unclear. OLP was induced in mice by transplanting human OLP lesions into the backs of thymus-free mice, and an in vitro cell model was constructed using LPS-stimulated HaCaT cells. Gene intervention was performed using shRNA lentiviral vectors. The secretion of the pro-inflammatory factors IL-6 and TNF-α, as well as the rate of apoptosis in HaCaT cells, was also assessed. ChIP assay and dual-luciferase assay were used to validate the transcriptional regulation of S100A7 by nuclear factor 1 A-type (NFIA). The expression of S100A7 was significantly elevated in the lesion tissues of OLP-induced mice. Knockdown of S100A7 alleviated inflammation and reduced keratinocyte apoptosis. The transcription factor NFIA repressed S100A7 expression by binding to the S100A7 promoter. The overexpression of NFIA ameliorated inflammation in vivo and reduced apoptosis in vitro, which was abrogated by further overexpression of S100A7. Overall, our results indicate that NFIA reduces inflammatory response-induced keratinocyte apoptosis in OLP by inhibiting S100A7 transcription.