Department of Stomatology, Hunan Provincial People's Hospital (The First Affiliated Hospital of Hunan Normal University), Changsha, 410000, China.
Biochem Biophys Res Commun. 2021 Dec 3;581:46-52. doi: 10.1016/j.bbrc.2021.09.081. Epub 2021 Oct 2.
Excessive inflammation leads to periodontitis, which inhibits the osteogenic differentiation of human dental pulp stem cells (hDPSCs), irreversibly injured and difficultly repaired for the important dental pulp. Hence, it is necessary to study the functional gene to enhance the osteogenic differentiation of hDPSCs. Previous found that SNHG7 expression was increased in the osteogenic differentiation of hDPSCs. However, the regulatory functions of SNHG7 on osteogenic differentiation of hDPSCs in the inflammatory microenvironment still remains unknown. In this study, hDPSCs treatment with 50 ng/mL TNF-α to mimic the inflammatory microenvironment, then cultured in osteoblast differentiation medium for 14 days. SNHG7, miR-6512-3p, BSP, DSPP, DMP-1, RUNX2 and OPN in hDPSCs were detect by RT-qPCR. We found that SNHG7 expression was reduced during the osteogenic differentiation of hDPSCs after different concentrations TNF-α treatment. SNHG7 overexpression improved the TNF-α-induced suppression of calcium deposition, ALP activity, and the expression of BSP, DSPP, DMP-1, RUNX2 and OPN. Furthermore, SNHG7 can sponge with miR-6512-3p. miR-6512-3p expression was increased during the osteogenic differentiation of hDPSCs after different concentrations TNF-α treatment while inhibited after SNHG7 overexpression. knockdown of miR-6512-3p improved the TNF-α-induced suppression of calcium deposition, ALP activity, and the expression of BSP, DSPP, DMP-1, RUNX2 and OPN. Finally, miR-6512-3p overexpression reversed the effect of SNHG7 on the osteo/dentinogenic differentiation of TNF-α-treated hDPSCs. In conclusions, SNHG7 improves the osteogenic differentiation of hDPSCs by inhibiting miR-6512-3p expression under 50 ng/mL TNF-α-induced inflammatory environment, which provided potential targets for the treatment of periodontitis.
过度炎症会导致牙周炎，抑制人牙髓干细胞（hDPSCs）的成骨分化，对重要的牙髓不可逆损伤且难以修复。因此，有必要研究功能基因以增强 hDPSCs 的成骨分化。先前发现 SNHG7 在 hDPSCs 的成骨分化中表达增加。然而，SNHG7 在炎性微环境中对 hDPSCs 成骨分化的调节功能仍不清楚。在这项研究中，用 50ng/mL TNF-α处理 hDPSCs 以模拟炎性微环境，然后在成骨分化培养基中培养 14 天。通过 RT-qPCR 检测 hDPSCs 中的 SNHG7、miR-6512-3p、BSP、DSPP、DMP-1、RUNX2 和 OPN。我们发现，在不同浓度 TNF-α处理后，hDPSCs 的成骨分化过程中 SNHG7 的表达减少。SNHG7 的过表达改善了 TNF-α 诱导的钙沉积、ALP 活性以及 BSP、DSPP、DMP-1、RUNX2 和 OPN 的表达抑制。此外，SNHG7 可以与 miR-6512-3p 结合。在不同浓度 TNF-α处理后，hDPSCs 的成骨分化过程中 miR-6512-3p 的表达增加，而过表达 SNHG7 后则受到抑制。miR-6512-3p 的敲低改善了 TNF-α 诱导的钙沉积、ALP 活性以及 BSP、DSPP、DMP-1、RUNX2 和 OPN 的表达抑制。最后，miR-6512-3p 的过表达逆转了 SNHG7 对 TNF-α 处理的 hDPSCs 成骨/牙本质分化的影响。总之，在 50ng/mL TNF-α 诱导的炎性环境下，SNHG7 通过抑制 miR-6512-3p 的表达来改善 hDPSCs 的成骨分化，为治疗牙周炎提供了潜在的靶点。
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