标题：Long noncoding RNA MALAT1 alleviates lipopolysaccharide-induced inflammatory injury by upregulating microRNA-19b in murine chondrogenic ATDC5 cells
作者：Pan, Lin; Liu, Deheng; Zhao, Lei; Wang, Liqin; Xin, Miaomiao; Li, Xingfu
作者机构：[Pan, Lin; Li, Xingfu] Shandong Univ, Dept Rheumatol, Qilu Hosp, 107 Wenhua West Rd, Jinan 250012, Shandong, Peoples R China.; [Pan, Lin; Zhao, Lei; 更多
通讯作者地址：[Li, XF]Shandong Univ, Dept Rheumatol, Qilu Hosp, 107 Wenhua West Rd, Jinan 250012, Shandong, Peoples R China.
来源：JOURNAL OF CELLULAR BIOCHEMISTRY
关键词：lipopolysaccharide; metastasis-associated lung adenocarcinoma transcript; 1; microRNA-19b; nuclear factor kappa B pathway; osteoarthritis;; Wnt/beta-catenin pathway
摘要：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-1 beta (IL)-1 beta, IL-6, IL-8, tumor necrosis factor alpha (TNF-alpha), 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-1 beta, IL-6, IL-8, and TNF-alpha in culture supernatant of ATDC5 cells. Expressions of key factors involved in cell apoptosis, proinflammatory response, Wnt/beta-catenin, and nuclear factor kappa B (NF-kappa B) 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/beta-catenin and NF-kappa B 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/beta-catenin and NF-kappa B 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.