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在炎症性微环境下,FTO通过SMOC2在人体干细胞中从上卵泡中积极调节牙质分化

Qi Huang^1,2,3, Yumei Sun^1,2,3, Wushuang Huang^1,2,3

¹Hospital of Stomatology, Sun Yat-sen University, Guangzhou 510055, China.

International journal of molecular sciences

|April 13, 2024

概括

脂肪质量和与肥胖相关的蛋白质 (FTO) 促进了人类干细胞从上乳头 (hSCAPs) 的牙芽细胞分化. FTO对抗炎症诱导的抑制,表明其在根部发育中的治疗潜力.

科学领域:

生物材料科学生物材料科学
干细胞生物学干细胞生物学
恢复性牙科恢复性牙科

背景情况:

人类干细胞与上乳头 (hSCAPs) 的牙芽细胞分化对于根部发育和牙形成至关重要,特别是在上牙周炎 (AP) 的未成熟牙中.
已知脂肪质量和与肥胖相关的蛋白质 (FTO) 影响骨再生和骨质分化,但其在hSCAPs中的作用尚未被理解.

研究的目的:

在正常和炎症条件下,研究FTO在hSCAPs的口腔细胞分化中的功能.
探索FTO影响hSCAPs差异化的潜在分子机制.

主要方法:

在诱导AP的老鼠身上进行组织学染色和微型计算机断层扫描 (微型CT),以评估根部发育和FTO表达.
使用性酸酶和阿里沙林红色S染色,qRT-PCR和西式斑点的hSCAPs差异化的体外评估.
对FTO和分泌的模块化结合蛋白2 (SMOC2) 的功能增益和丧失测定,以及生物信息学分析.

主要成果:

有AP的老鼠表现出FTO表达的下调和根部发育缺陷.
在体外hSCAPs分化过程中FTO表达增加;脂多糖 (LPS) 抑制了FTO和分化.
FTO过度表达减轻了LPS诱导的抑制,促进了SMOC2表达,这部分介导了FTO促进差异化的效果.

结论:

通过增强SMOC2表达,FTO积极调节hSCAPs的口腔细胞分化.
由LPS引起的炎症通过降低FTO的调节来损害hSCAPs的分化.
在炎症条件下,FTO显示为调节hSCAPs分化的治疗标.

关键词:

脂肪质量和与肥胖相关的蛋白质.人类的干细胞来自于状乳头.这是一种炎症炎症炎症炎症.牙芽细胞分化的差异化分泌的模块化结合蛋白2 分泌

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