关键词: SNHG1 autophagy human dental follicle stem cells osteogenic differentiation oxidative stress

Mesh : Humans RNA, Long Noncoding / genetics metabolism Autophagy / genetics Oxidative Stress / genetics Osteogenesis / genetics Cell Differentiation / genetics Stem Cells / metabolism Dental Sac / metabolism cytology Enhancer of Zeste Homolog 2 Protein / metabolism genetics Epigenesis, Genetic Cells, Cultured Gene Knockdown Techniques

来  源:   DOI:10.1002/jcp.31283

Abstract:
The long noncoding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) plays a crucial role in tumorigenesis and is frequently employed as a prognostic biomarker. However, its involvement in the osteogenic differentiation of oral stem cells, particularly human dental follicle stem cells (hDFSCs), remains unclear. Our investigation revealed that the absence of SNHG1 enhances the osteogenic differentiation of hDFSCs. Furthermore, the downregulation of SNHG1 induces autophagy in hDFSCs, leading to a reduction in intracellular oxidative stress levels. Notably, this effect is orchestrated through the epigenetic regulation of EZH2. Our study unveils a novel function of SNHG1 in governing the osteogenic differentiation of hDFSCs, offering fresh insights for an in-depth exploration of the molecular mechanisms underlying dental follicle development. These findings not only provide a foundation for advancing the understanding of SNHG1 but also present innovative perspectives for promoting the repair and regeneration of periodontal supporting tissue, ultimately contributing to the restoration of periodontal health and tooth function.
摘要:
长非编码RNA(lncRNA)小核仁RNA宿主基因1(SNHG1)在肿瘤发生中起着至关重要的作用,并且经常被用作预后生物标志物。然而,它参与口腔干细胞的成骨分化,特别是人类牙囊干细胞(hDFSCs),尚不清楚。我们的研究表明,SNHG1的缺失增强了hDFSCs的成骨分化。此外,SNHG1的下调诱导hDFSCs的自噬,导致细胞内氧化应激水平降低。值得注意的是,这种效应是通过EZH2的表观遗传调控来协调的。我们的研究揭示了SNHG1在控制hDFSCs成骨分化方面的新功能,为深入探索牙囊发育的分子机制提供新的见解。这些发现不仅为促进对SNHG1的理解提供了基础,而且为促进牙周支持组织的修复和再生提供了创新的观点。最终有助于牙周健康和牙齿功能的恢复。
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