RETRACTED: MicroRNA-145 attenuates IL-6-induced enhancements of sensitivity to UVB irradiation by suppressing MyD88 in HaCaT cells

Abstract

MicroRNAs (miRNAs/miRs) play vital roles in various immune diseases including systemic lupus erythematosus (SLE). The current study aimed to assess the role of miR-145 in interleukin-6 (IL-6)-treated HaCaT cells under ultraviolet B (UVB) irradiation and further explore the potential regulatory mechanism. HaCaT cells were pretreated with IL-6 and then exposed to UVB to assess the effect of IL-6 on sensitivity of HaCaT cells to UVB irradiation. The levels of miR-145 and MyD88 were altered by transfection and the transfected efficiency was verified by quantitative reverse transcription polymerase chain reaction (qRT-PCR)/western blot analysis. Cell viability, percentage of apoptotic cells and expression levels of apoptosis-related factors were measured by trypan blue assay, flow cytometry assay, and western blot analysis, respectively. In addition, the levels of c-Jun N-terminal kinases (JNK) and nuclear factor-κB (NF-κB) signaling pathway-related factors were assessed by western blot analysis. IL-6 treatments significantly aggravated the reduction of cell viability and promotion of cell apoptosis caused by UVB irradiation in HaCaT cells. Interestingly, miR-145 level was augmented by UVB exposure and miR-145 mimic alleviated IL-6-induced increase of sensitivity to UVB irradiation in HaCaT cells, as dramatically increased cell viability and reduced cell apoptosis. Opposite effects were observed in miR-145 inhibitor-transfected cells. Meanwhile, MyD88 was negatively regulated by miR-145 and MyD88 mediated the regulatory effect of miR-145 on IL-6- and UVB-treated cells. In addition, miR-145 mimic inhibited the JNK and NF-κB pathways by down-regulating MyD88. In conclusion, the present study demonstrated that miR-145 alleviated IL-6-induced increase of sensitivity to UVB irradiation by down-regulating MyD88 in HaCaT cells.

Anti-antioxidant impacts of circZNF609 silence in HaCaT cells through regulating miR-145

“…For instance, miR-145 was low expressed in psoriatic lesional skin [30]. Of contrast, high expression of miR-145 was observed in a cell model of systemic lupus erythematosus [31] as well as various nonmelanoma skin cancers like basal cell carcinoma and squamous cell carcinoma [32]. The present paper illustrated the low expressed miR-145 in the cell model of pressure ulcer, which was established by stimulating HaCaT cells with H 2 O 2 .…”

MiR-664 Protects Against UVB Radiation-Induced HaCaT Cell Damage via Downregulating ARMC8

“…27 MicroR-145 alleviates interleukin-6-induced increase in sensitivity to UVB irradiation by downregulating MyD88 in HaCaT cells. 28 Ultraviolet B irradiation inhibits iASPP (Inhibitor of Apoptosis Stimulating Protein of p53) expression through inducing miR-340 expression, thereby promoting RPE cell apoptosis and suppressing cell proliferation. 29 In our present study, we found that the expression of miR-664 upregulated in UVB-radiated HaCaT cells.…”

IL6R is a target of miR‐197 in human keratinocytes

“…The concentrations we have chosen to use, 5-50 ng/mL of IL-6, were according to previous work which shows the biochemical and biological effects of IL-6 in keratinocytes. [45][46][47][48] PHK cells were treated with IL-6 at several different conditions of…”