Knockdown of lncRNA JPX suppresses IL‑1β‑stimulated injury in chondrocytes through modulating an miR‑25‑3p/PPID axis

Abstract

The aim of this study was to investigate the potential mechanisms of long noncoding (lnc) RNA Just proximal to X-inactive specific transcript (JPX) in interleukin (IL)-1β-stimulated chondrocytes. Human C28/I2 chondrocytes were treated with IL-1β to simulate osteoarthritic (OA) injury. The expression levels of JPX, microRNA (miRNA/miR)-25-3p, and peptidylprolyl isomerase D (PPID) were measured using reverse transcription-quantitative PCR or western blotting. The IL-1β-stimulated injury was assessed using a Cell Counting Kit-8 assay, flow cytometry, and western blot analysis. The targeted relationship between miR-25-3p, JPX, and PPID was verified using a dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. The results showed that JPX expression was upregulated in OA patients and IL-1β-stimulated chondrocytes. JPX knockdown enhanced cell viability and suppressed apoptosis of IL-1β-stimulated chondrocytes. miR-25-3p inhibition rescued the inhibitory effect of JPX knockdown on IL-1β-stimulated injury. PPID overexpression eliminated the effects of JPX knockdown on IL-1β-stimulated chondrocytes. In conclusion, JPX knockdown increased cell viability and reduced apoptosis in IL-1β-stimulated chondrocytes, and this involved modulation of a miR-25-3p/PPID axis.

Suppression of lncRNA OIP5-AS1 Attenuates Apoptosis and Inflammation, and Promotes Proliferation by Mediating miR-25-3p Expression in Lipopolysaccharide-Induced Myocardial Injury

“…MiR-25-3p has also been reported to interact with various lncRNAs in diverse diseases [30][31][32][33]. LncRNA can act as competitive endogenous RNA via directly sponging target miRNAs.…”