The Impact and Mechanisms of LncRNA TCONS_00483150 on the Function of Self-Reactive B Cells in Systemic Lupus Erythematosus

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Abstract

Background: Excessive proliferation and activation of B cells, resulting in the production of various autoantibodies, is a crucial link and significant feature of the pathogenesis of systemic lupus erythematosus (SLE). Accumulating evidence indicated that long non-coding RNAs (lncRNAs) play a significant role in SLE. TCONS_00483150 is reported as a novel diagnostic biomarker that recently reported as a potential for SLE. However, the detailed functions and mechanisms are unclear. This study aimed to investigate the effects of TCONS_00483150 on B cell function and SLE progression. Methods: B cells were administrated with TCONS_00483150 overexpression and JAK activator. The activation of B cells was measured by flow cytometry. The production of IgG and IgM antibodies was measured by ELISA assay. The protein expression was assessed by western blot. Cell viability, cell cycle, and apoptosis were measured by cell counting kit-8 (CCK-8) and flow cytometry. Results: Overexpression of TCONS_00483150 led to deceased portion of CD19+CD138+ B cells and suppressed the expression of BAFF and APRIL. The production of IgG and IgM was significantly suppressed by TCONS_00483150 overexpression. TCONS_00483150 suppressed the viability and cell portion in S phase, as well as promoted the apoptosis of B cells. Overexpression of TCONS_00483150 suppressed the phosphorylation of the JAK and STAT3 protein. Treatment with STAT3 activator notably increased the viability of B cells and suppressed cell apoptosis, whereas overexpression of TCONS_00483150 repressed these effects. Conclusion: TCONS_00483150 overexpression could suppress the proliferation and activation of B cells, potentially via suppressing the activation of JAK/STAT3.

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