Long noncoding RNA MALAT1 alleviates lipopolysaccharide‐induced inflammatory injury by upregulating microRNA‐19b in murine chondrogenic ATDC5 cells

Osteoarthritis is the most frequent chronic bone‐joint disease in middle‐aged and older people worldwide. This study investigated the effects of long noncoding RNA metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1) on lipopolysaccharide (LPS)‐induced murine chondrogenic ATDC5 cell inflammatory injury. Cell viability and apoptosis were assessed using cell counting kit‐8 assay and annexin V‐phycoerythrin (PE) staining, respectively. The expression levels of interleukin‐1β (IL)‐1β, IL‐6, IL‐8, tumor necrosis factor α (TNF‐α), MALAT1, and microRNA‐19b (miR)‐19b were measured using quantitative reverse‐transcription polymerase chain reaction. Enzyme‐linked immunosorbent assay was conducted to detect the concentrations of IL‐1β, IL‐6, IL‐8, and TNF‐α in culture supernatant of ATDC5 cells. Expressions of key factors involved in cell apoptosis, proinflammatory response, Wnt/β‐catenin, and nuclear factor κB (NF‐κB) pathways were analyzed using Western blot analysis. We found that LPS treatment remarkably induced ATDC5 cell apoptosis and inflammatory injury. MALAT1 was upregulated in LPS‐stimulated ATDC5 cells. Overexpression of MALAT1 significantly reversed the LPS‐induced ATDC5 cell inflammatory injury, while suppression of MALAT1 had opposite effects. Further results showed that MALAT1 positively regulated the expression of miR‐19b in ATDC5 cells. Knockdown of miR‐19b reversed the protective effect of MALAT1 on LPS‐induced ATDC5 cells. In addition, MALAT1 reduced LPS‐induced Wnt/β‐catenin and NF‐κB pathways activation in ATDC5 cells by upregulating miR‐19. To conclude, our research verified that MALAT1 alleviated LPS‐induced ATDC5 cell inflammatory injury by upregulating miR‐19b and inactivating Wnt/β‐catenin and NF‐κB pathways. This finding will be helpful for further understanding the critical roles of MALAT1 and miR‐19b in osteoarthritis and may provide possible targets for osteoarthritis diagnosis and treatment. The effects of metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1) and microRNA (miR)‐19b on lipopolysaccharide (LPS)‐induced activation of Wnt/β‐catenin and nuclear factor κB (NF‐κB) pathways were also analyzed. This finding will be helpful for further understanding the critical roles of MALAT1 and miR‐19b in osteoarthritis and may provide possible therapeutic and diagnostic targets for osteoarthritis treatments.