Elevated expression of lncRNA SNHG15 in spinal tuberculosis: preliminary results.

OBJECTIVE:The incidence and disability rate of spinal tuberculosis is high. The role of the expression of lncRNA SNHG15 in spinal tuberculosis and related mechanisms remains unclear. PATIENTS AND METHODS:Spinal tuberculosis and normal control tissues were collected, and lncRNA SNHG15 level was analyzed by real-time PCR. Mouse RAW264.7 cells were cultured and divided into control group, tuberculin (PPD) group, si-SNHG15, and PPD+ si-SNHG15 group followed by analysis of lncRNA SNHG15 level, cell proliferation by MTT assay, formation of osteoclasts by TRAP staining, levels of interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) by ELISA, as well as expression of RANK and RANKL by Western blot. RESULTS:The lncRNA SNHG15 expression in spinal tuberculosis tissues was significantly increased compared with that in the control group (p < 0.05). The expression of lncRNA SNHG15 was increased in RAW264.7 cells in the PPD group with increased cell proliferation, TRAP-positive cells, IL-6 and TNF-α secretion, as well as elevated RANK and RANKL expression which were statistically different compared with the control group (p < 0.05). Transfection of lncRNA SNHG15 siRNA in the PPD model significantly inhibited the expression of lncRNA SNHG15, decreased cell proliferation, TRAP staining positive cells, IL-6 and TNF-α secretion, as well as reduced RANK and RANKL expression. Compared with the PPD group, the differences were statistically significant (p < 0.05). CONCLUSIONS:The expression of lncRNA SNHG15 was significantly increased in spinal tuberculosis tissues. The downregulation of lncRNA SNHG15 expression could inhibit the secretion of inflammatory cytokines by regulating the RANK/RANKL pathway, thereby regulating osteoclasts.

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