MicroRNA-939 amplifies induced matrix metalloproteinase expression in atopic dermatitis.

BACKGROUND

Atopic dermatitis (AD) is a common chronic inflammatory skin diseases that seriously affects life quality of the patients. () colonization on the skin plays an important role in the pathogenesis of AD; however, the mechanism of how it modulates skin immunity to exacerbate AD remains unclear. MicroRNAs are short non-coding RNAs that act as post-transcriptional regulators of genes. They are involved in the pathogenesis of various inflammatory skin diseases.

METHODS

In this study, we established miRNA expression profiles for keratinocytes stimulated with heat-killed (HKSA). The expression of miR-939 in atopic dermatitis patients was analyzed by fluorescence in situ hybridization (FISH). miR-939 mimic was transfected to human primary keratinocyte to investigate its impact on the expression of matrix metalloproteinase genes (MMPs) . Subsequently, miR-939, along with Polyplus transfection reagent, was administered to MC903-induced atopic dermatitis skin to assess its function .

RESULTS

MiR-939 was highly upregulated in HKSA-stimulated keratinocytes and AD lesions. studies revealed that miR-939 increased the expression of matrix metalloproteinase genes, including MMP1, MMP3, and MMP9, as well as the cell adhesion molecule ICAM1 in human primary keratinocytes. studies indicated that miR-939 increased the expression of matrix metalloproteinases to promote the colonization of and exacerbated -induced AD-like skin inflammation.

CONCLUSIONS

Our work reveals miR-939 is an important regulator of skin inflammation in AD that could be used as a potential therapeutic target for AD.