Effects of LncRNA MALAT1 on proliferation,apoptosis and inflammatory response of mesangium cells in mice with lupus nephritis
Objective To investigate the effects of long non-coding RNA(LncRNA)metastasis-associated transcripton-1 (MALAT1)on the proliferation,apoptosis,inflammatory response and Notch2/hes1 pathway of mesangial cells(MC)in mice with lu-pus nephritis(LN).Methods Ten MRL/MPJ-FASLPR mice were selected as LN group and five healthy MRL/MpJ mice were se-lected as normal group.They were divided into Mock group(normal culture),Vector group(control after transfection MALAT1 overex-pression empty vector pcDNA3.1),MALAT1 group(transfection MALAT1 overexpression),SiNC group(transfection with low Si-MALAT1 negative control SiNC),SIMalat1-1/2/3 groups(transfection SiMAL AT1-1/2/3).Real-time fluorescence quantitative PCR (qRT-PCR)was used to detect MALAT1 expression in kidney tissue and MC cells of mice in normal and LN groups.CCK-8 and EdU methods was used to detect the effect of MALAT1 on the proliferation of MC cells.Flow cytometry was used to detect the apoptosis of MC cells in each group.ELISA was used to detect the levels of tumor necrosis factor α(TNF-α),interleukin-1β(IL-1β)and IL-6 in MC cells.Western Blot was used to detect the effects of MALAT1 on proliferation,apoptosis and proteins associated with Notch2/hes1 signaling pathway of MC cells.Results MALAT1 was highly ex-pressed in kidney tissue of LN mice (P<0.05).Overexpression of MALAT1 could promote the proliferation and inflammation of MC cells,induce apoptosis,and up-regulate the protein levels of Notch2 and hes1.MALAT1 knockdown had the opposite effect to MALAT1 overexpression (P<0.05).Conclusion MALAT1 knockdown can inhibit the proliferation and inflammatory response of MC cells in LN mice and induce apoptosis.The mechanism may be related to the inhibition of Notch2/hes1 signaling pathway.
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