MicroRNA-139-5p alleviates UVB-induced injuries by regulating TLR4 in si-IL-6-treated keratinocyte cells.

Background: Lupus erythematosus (LE) is an autoimmune disease that is often exacerbated by ultraviolet B (UVB) irradiation. MicroRNAs (miRNAs) play vital roles in response to UVB damage to keratinocyte cells. Herein, our study aimed to explore the functions of miR-139-5p in UVB-induced injuries in keratinocyte cells.

Methods: Human keratinocyte cell line HaCaT was per-treated with 20 ng/ml si-IL-6 and transfected with miR-139-5p mimic, pc-TLR4 and corresponding controls. These cells were underwent 30 mJ/cm2 UVB irradiation and incubated for 24 h. Thereafter, cell viability and apoptosis were detected by trypan blue staining and flow cytometry assays. Furthermore, the expression levels of miR-139-5p, TLR4, apoptosis-associated factors, Notch and PI3K/AKT pathways factors were examined by qRT-PCR and western blot.

Results: Our results showed that UVB irradiation pronouncedly enhanced si-IL-6-induced cell injuries, as decreased cell viability and promoted apoptosis in HaCaT cells. In addition, miR-139-5p was up-regulated in UVB-exposed HaCaT cells and overexpression of miR-139-5p attenuated UVB-induced injuries in si-IL-6-treated HaCaT cells. Further study we found that overexpression of TLR4 significantly abolished the protective effects of miR-139-5p overexpression against UVB-induced injuries in si-IL-6-treated HaCaT cells. Besides, western blot results demonstrated that overexpression of miR-139-5p inactivated Notch and PI3K/AKT pathways by down-regulation of TLR4.

Conclusions: These results indicated that miR-139-5p alleviated UVB-induced injuries by regulation of TLR4 in si-IL-6-treated HaCaT cells. The study might provide new therapeutic strategies for treatment of LE.