MiR-494 alleviates lipopolysaccharide (LPS)-induced autophagy and apoptosis in PC-12 cells by targeting IL-13

Background. MiR-494 is reported to act as a tumor-suppressive factor that inhibits the proliferation and colony formation of some cancer cells. However, there is still no report available on miR-494 functions in spinal cord injury (SCI) until now. Objectives. The objective of this study was to examine the status of miR-494 in PC-12 cells injury induced by lipopolysaccharide (LPS), as well as its mechanism. Material and methods. The cell counting kit-8 (CKK-8) assay and apoptosis assay were respectively used to determine the proliferation and apoptosis of PC-12. The reverse transcription polymerase chain reaction (RT-PCR) analysis and western blot analysis displayed the expression of related factors at mRNA and protein level, respectively. Results. The results showed that LPS could significantly decrease cell viability, and promote the cell apoptosis and autophagy of PC-12 in a dose-dependent manner (p < 0.05). The overexpression of miR-494 could protect PC-12 cells from LPS-induced injury, as miR-494 overexpression increased cell viability, and reduced cell apoptosis and autophagy (p < 0.05). MiR-494 played a negative regulatory role in interleukin (IL)-13, and IL-13 was a direct target of miR-494. The overexpression of IL-13 could significantly aggravate LPS-diminished cell viability, and LPS-induced apoptosis and autophagy (p < 0.05). Besides, the overexpression of miR-494 did not attenuate LPS-induced injury when IL-13 was overexpressed. Furthermore, we found that the overexpression of miR-494 could significantly promote the phosphorylation of STAT6/MAPK and ERK/JNK signaling pathway. Conclusions. MiR-494 could protect PC-12 cells from LPS-induced cell damage by targeting IL-13, and the activation of STAT6/MAPK and ERK/JNK pathways.