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Long non-coding RNA TUG1 protects renal tubular epithelial cells against injury induced by lipopolysaccharide via regulating microRNA-223.

BACKGROUND: Lupus nephritis (LN) is a serious complication of systemic lupus erythematosus (SLE). Long non-coding RNA taurine upregulated gene 1 (lncRNA TUG1) exerted critical regulatory effects on inhibiting cell injury and inflammation. However, its role in LN is still unclear.

METHODS: HK-2 cells were treated with lipopolysaccharide (LPS) to simulate cell inflammatory injury. Cell viability and apoptosis, as well as pro-inflammatory factors expression were measured, respectively. Then, HK-2 cells were transfected with pEX-TUG1 or sh-TUG1 to explore the effects of TUG1 on LPS-induced cell injury. Potential binding effects between TUG1 and microRNA-223 (miR-223), as well as between miR-223 and Sirtuin 1 (Sirt1) were verified. miR-223 mimic or miR-223 inhibitor was transfected to assess the effects of miR-223 on cell injury. Finally, the roles of Sirt1 in LPS-induced HK-2 cell injury and activation of phosphatidylinositol 3-kinase/protein kinase 3 (PI3K/AKT) and nuclear factor kappa B (NF-κB) pathways were explored.

RESULTS: LPS administration inhibited HK-2 cell viability and proliferation, increased expression of pro-inflammatory factors, and promoted cell apoptosis. TUG1 overexpression protected HK-2 cells against LPS-induced injury via negatively regulating miR-223 expression. TUG1 suppression had opposite effects. Sirt1 was a direct target gene of miR-223 in HK-2 cells, which participated in the effects of miR-223 on HK-2 cells and was related with the activation of PI3K/AKT and NF-κB pathways.

CONCLUSION: TUG1 protected HK-2 cells against LPS-induced inflammatory injury by regulating miR-223 and Sirt1 expression, and then activating PI3K/AKT and inactivating NF-κB pathways. TUG1 might be a potential therapeutic target for LN treatment.

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