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

Abstract

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.

Retracted: Lipopolysaccharides‐mediated injury to chondrogenic ATDC5 cells can be relieved by Sinomenine via downregulating microRNA‐192

“…First, ATDC5 cells were subjected to LPS to mimic an in vitro model of OA. In line with previous studies (Pan et al, ; Wang & Kong, ; Zhu et al, ), LPS induced a significant cell loss and pro‐inflammatory cytokines release, indicating ATDC5 cells were injured by LPS, and the cell model of OA was established successfully. Further experiments found that SIN treatment attenuated LPS‐induced cell injury, and the functional effects of SIN were implicated with the decreased expression of miR‐192 by SIN.…”

“…The objective of this study was to study the effects of SIN on mouse chondrogenic ATDC5 cells growth and inflammation and tried to reveal one of the possible underlying mechanisms. To this end, ATDC5 cells were subjected to lipopolysaccharide (LPS) to mimic an in vitro model of OA as previously described (Pan et al, ; Wang & Kong, ; Zhu, Wang, Teng, Chen, & Pan, ). Subsequently, ATDC5 cells were treated by SIN to see the effects of SIN on LPS injury to ATDC5 cells.…”

Clinical significance of miR-19b-3p in patients with sepsis and its regulatory role in the LPS-induced inflammatory response

“…As Qiao et al [16] reported, miR-19b-3p alleviated LPS-induced inflammatory injury in human intestinal cells through regulating PI3K/AKT signaling pathways. Another study in osteoarthritis reported that miR-19b-3p was involved in the regulation of LPS-induced murine chondrogenic cell inflammatory injury by inactivating Wnt/β-catenin and NF-κB pathways [30]. It is known that the endothelium plays a crucial role in health and disease, and endothelial dysfunction has been determined to contribute to sepsis pathophysiology [3].…”

Therapeutic potential of extracellular vesicle‐associated long noncoding RNA

“…32 The same group explored the molecular action of KLF3-AS1 and found that it sponges miR-206 leading to the upregulation of G-protein-coupled receptor kinase interacting protein-1 and resulting in chondrocyte proliferation and apoptosis inhibition. 33 35 Osteoporosis is characterized by skeletal fragility and microarchitectural deterioration, 36 and differentiating bone marrow stromal cells to osteoblasts as a treatment has been an active area of research. 37,38 Zhang et al showed that osteogenic differentiation of bone marrow-derived MSCs was promoted by lncRNA NEAT1 via sponging miR29b-3p to upregulate BMP1.…”