SNHG1 knockdown promotes osteogenic differentiation of hDFSCs through anti-oxidative stress mediated by autophagy

Area of Science:

• Stem Cell Biology
• Molecular Biology
• Biomaterials Science

Background:

• Long noncoding RNA (lncRNA) SNHG1 is implicated in tumorigenesis and serves as a prognostic biomarker.
• The role of SNHG1 in the osteogenic differentiation of oral stem cells, specifically hDFSCs, is not well understood.

Purpose of the Study:

• To investigate the function of SNHG1 in the osteogenic differentiation of human dental follicle stem cells (hDFSCs).
• To elucidate the molecular mechanisms by which SNHG1 influences hDFSC osteogenesis and autophagy.

Main Methods:

• Quantitative real-time PCR to assess SNHG1 expression.
• Alkaline phosphatase activity assays and Alizarin Red S staining to evaluate osteogenic differentiation.
• Western blotting to detect autophagy-related proteins and EZH2 expression.
• Autophagy flux assays and reactive oxygen species (ROS) detection.

Main Results:

• SNHG1 downregulation significantly enhanced the osteogenic differentiation of hDFSCs.
• Reduced SNHG1 expression induced autophagy and decreased intracellular oxidative stress in hDFSCs.
• SNHG1's effects were mediated through the epigenetic regulation of Enhancer of Zeste Homolog 2 (EZH2).

Conclusions:

• SNHG1 negatively regulates the osteogenic differentiation of hDFSCs.
• Downregulation of SNHG1 promotes autophagy and reduces oxidative stress via EZH2 epigenetic modulation.
• These findings provide novel insights into dental follicle development and potential therapeutic strategies for periodontal regeneration.