BackgroundThe dramatic increase of intervertebral disc degeneration (IDD) is considered to be a major cause of discogenic low back pain. The current study focused on the regulatory function of microRNA-194 (miR-194) on lipopolysaccharide (LPS)-induced inflammatory response in nucleus pulposus (NP) cells.Material/MethodsLPS was used to treat NP cells to induce inflammatory responses. MiRNA and gene expression were detected by quantitative PCR. Proteins and protein expression levels were detected by Western blot and ELISA kit. Dual luciferase reporter assay was applied to identify the correlation between an miR-194- and TNF receptor-associated factor 6 (TRAF6) and to test NF-κB activity.ResultsMiR-194 expression was reduced in LPS-induced NP cells. Both miR-194 overexpression and miR-194 inhibitor could regulate extracellular matrix (ECM) genes expression (Aggrecan and collagen II), MMP3, MMP13, ADAMTS4, and ADAMTS5, as well as inflammatory cytokines-associated genes (TNF-α, IL-1, IL-6, PGE2). Through a further study of the molecular mechanism, miR-194 was proved to be involved in the regulation of TRAF6 and its downstream signal molecule, nuclear factor-kappa B (NF-κB).ConclusionsFinding of our study suggest that miR-194 can inhibit LPS-induced inflammatory response in NP cells of the intervertebral disc (IVD) by targeting TRAF6, which may contribute development of IDD biological therapy.

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Background. Retinoblastoma (RB) is the commonest primary intraocular malignancy during childhood. Circular RNAs (circRNAs) act as regulators in RB development, and hsa_circ_E2F5 (circ_0084811 in this study) was found to be highly expressed in RB cells, so we wanted to identify its detailed molecular mechanism. Methods. The expression level of circ_0084811 in RB cells was tested by RT-qPCR and its effects on RB cells were evaluated through functional assays. The regulatory mechanism that circ_0084811 may exert in RB progression was testified through mechanism experiments. Results. High circ_0084811 expression in RB cells facilitated cell proliferation but inhibited cell apoptosis. The enrichment of acetylation of histone 3 lysine 27 (H3K27ac) in circ_0084811 promoter induced circ_0084811 upregulation. Moreover, circ_0084811 regulated E2F transcription factor 5 (E2F5) expression via sponging microRNA-18a-5p (miR-18a-5p) and microRNA-18b-5p (miR-18b-5p). Conclusion. circ_0084811 modulated RB progression via the miR-18a-5p/miR-18b-5p/E2F5 axis.