LncRNA OIP5-AS1 accelerates intervertebral disc degeneration by targeting miR-25-3p

Abstract

It is obvious that epigenetic processes influence the evolution of intervertebral disc degeneration (IDD). However, its molecular mechanisms are poorly understood. Long noncoding RNAs (lncRNAs) have been validated to exert vital roles in IDD. Therefore, we tested the hypothesis that OIP5-AS1, a potential regulator of IDD, modulates IDD progression. RT-PCR was utilized to detect levels of OIP5-AS1, miR-25-3p, Collagen II and Aggrecan in IDD tissues and nucleus pulposus cells (NPCs). Immunofluorescence assay measured Collagen II expression. CCK-8, EdU, and flow cytometry estimated the levels of proliferation and apoptosis. Proteins were assessed via Western blot. The binding affinity of OIP5-AS1 with miR-25-3p was investigated by luciferase reporter assay. Enzyme-linked immunosorbent assay (ELISA) analyzed the levels of inflammatory factors. OIP5-AS1 was high expressed in IDD tissues and its expression gradually promoted with the increasing of Pfirrmann scores. The cell morphology of NPCs changed into spindle-shaped, and Collagen II expression was low. After OIP5-AS1 was silenced, cell proliferation was boosted whereas both apoptosis and extracellular matrix (ECM) degradation were restrained. In LPS-activated NPCs, OIP5-AS1 depletion also suppressed inflammation response. Further, miR-25-3p was a target of OIP5-AS1. The effects of OIP5-AS1 silence on proliferation, apoptosis, and ECM degradation were reversed upon miR-25-3p downregulation. Moreover, the inhibitory impact of OIP5-AS1 knockdown on the inflammation of LPS-treated NPCs was rescued with miR-25-3p inference. In general, lncRNA OIP5-AS1 exerted its effects in IDD by targeting miR-25-3p, implying the usage of OIP5-AS1/miR-25-3p as a novel regulatory axis for the molecular targets of IDD therapy.

MECHANISM OF MIR-25-3P CARRIED BY EXTRACELLULAR VESICLES DERIVED FROM PLATELET-RICH PLASMA IN IL-1β–INDUCED NUCLEUS PULPOSUS CELL DEGENERATION VIA THE SOX4/CXCR7 AXIS

“…Extracellular vesicles derived from PRP can transport multiple bioactive substances, including miRs, proteins, and mRNAs to involve in intercellular communication (35,52). Interestingly, preceding studies reported that miR-25 regulated NP cell processes in IVD, and miR-25-3p targeted lncRNA OIP5-AS1 to modulate IVD degeneration (22,36). Herein, we proposed that miR-25-3p may be carried by PRP-EVs into NP cells and thus affect NP cell degeneration.…”

Knockdown of lncRNA PCAT6 suppresses the growth of non-small cell lung cancer cells by inhibiting macrophages M2 polarization via miR-326/KLF1 axis

“…Human IL1β (Interleukin 1 Beta) ELISA Kit or Human IL10 (Interleukin 10) ELISA Kit was used to detect the expressions of IL-1β or IL-10 in the supernatant of macrophage according to the manufacturer’s instructions. Human IL1β (Interleukin 1 Beta) ELISA Kit and Human IL10 (Interleukin 10) ELISA Kits were purchased from ELK Biotechnology according to the previous literature [ 43 ].…”

“…All experiments were repeated three times. P < 0.05 was regarded as significant difference according to the previous literature [ 43 ].…”

Curcumin relieved the rheumatoid arthritis progression via modulating the linc00052/miR-126-5p/PIAS2 axis

“…The cell viability was assessed with CCK8 and EdU assays [ 23 ]. The cells were seeded into a 96-well plate in the presence of various curcumin concentrations for 12, 24, 48, and 72 h. Then, 10 μL/well of CCK-8 reagent was added and the cells were cultured for 2 h. Absorbance was measured at a wavelength of 450 nm.…”