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.