LINC00265 Promotes IL-1β-Induced Chondrocyte Inflammation and Extracellular Matrix Degradation by Activating the MAPK/NF-κB Pathway

Abstract

Aim: To study the effect and mechanisms of long intergenic non-protein coding RNA 265 (LINC00265) on osteoarthritis (OA) progression. Methods: Cartilage tissues from OA patients who received knee arthroplasty and from patients with traumatic amputees not suffering from OA or rheumatoid arthritis (normal) were collected and LINC00265 was evaluated by qRT-PCR (quantitative real-time polymerase chain reaction). In addition, CHON-001 cells were treated and classified into 4 groups: Control group, IL-1β (interleukin 1β) group (10 ng/mL), IL-1β + sh-NC group and IL-1β + sh-LINC00265 group. Subsequently, qRT-PCR was applied to determine LINC00265 expression, and extracellular matrix (ECM) degradation-related genes (ADAMTS-5, MMP3, COL2A1 and aggrecan). CCK-8 (cell counting kit-8) was used to study cell viability;ELISA (enzyme linked immunosorbent assay) was used to measure the levels of inflammatory cytokines IL-8 and IL-6, as well as tumor necrosis factor (TNF-α). Related kits were employed to identify reactive oxygen species (ROS) levels;Western blot was utilized for identifying MAPK/NF-κB (mitogen-activated protein kinase/nuclear factor kappa-B) pathway-related protein expression in cells. Results: LINC00265 was notably up-regulated in cartilage tissues of OA patients. The stimulation of IL-1β in chondrocytes could promote the expression of LINC00265 and inflammatory factors, the occurrence of ROS, and the degradation of ECM. However, the knockdown of LINC00265 reduced inflammation, cell proliferation and oxidative stress-related factor levels stimulated by IL-1β, and slowed down the progression of ECM degradation. In addition, the knockdown of LINC00265 suppressed the IL-1β-induced stimulation of the MAPK/NF-κB pathway. Conclusions: LINC00265 is a potential key signaling molecule for ECM degradation and IL-1β-stimulated chondrocyte inflammation.