对转录组和蛋白质组的综合分析揭示了在氧化应激下参与骨质细胞的核心基因组
Yixin Mao1, Qianru Ye2, Shufan Zhao3
1Department of Prosthodontics, School and Hospital of Stomatology, Wenzhou Medical University, Wenzhou, 325027, China; Institute of Stomatology, School and Hospital of Stomatology, Wenzhou Medical University, Wenzhou, 325027, China; Laboratory for Myology, Department of Human Movement Sciences, Faculty of Behavioural and Movement Sciences, Vrije Universiteit Amsterdam (VUA), Amsterdam Movement Sciences, Amsterdam, 1081 HZ, Netherlands.
Biochemical and biophysical research communications
|November 10, 2024
概括
氧化应激会损害骨质母细胞的功能,导致骨质疏松症. 这项研究确定了七个关键基因参与了这种功能障碍,提供了有关骨形成障碍的见解.
科学领域:
- 生物化学 生物化学
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
背景情况:
- 由于氧化应激 (OS) 的骨质细胞功能障碍是骨质疏松症发展的关键因素.
- 在OS下调节骨质母细胞功能障碍的特定基因尚未完全理解.
研究的目的:
- 为了研究OS对骨质母细胞表型的影响.
- 通过转录组和蛋白质组分析,识别和描述参与OS诱导的骨质母细胞功能障碍的基因和蛋白质.
主要方法:
- 使用过氧化 (H2O2) 诱导的骨质细胞功能障碍模型.
- 进行了转录组和蛋白质组分析,以确定差异表达基因 (DEG) 和蛋白质 (DEP).
- 构建了一个蛋白质-蛋白质相互作用 (PPI) 网络和集成的mRNA-蛋白质表达数据.
主要成果:
- 鉴定了164个DEG和186个DEP,富含着亡和骨质细胞分化途径.
- 鉴定了七个关键基因 (Ho-1,Fosl1,Fosl2,Ccnd2,Col1α1,Col12α1,Fgfr2) 与相关的mRNA和蛋白质表达.
- 发现Ho-1,Fosl1和Fosl2被上调,而Ccnd2,Col1α1,Col12α1和Fgfr2被下调,影响细胞周期,细胞亡和分化.
结论:
- 确定了7个候选基因,可能会调解OS对骨质细胞亡和功能障碍的有害影响.
- 这些发现为OS诱导的骨形成障碍和骨质疏松症病原体提供了新的见解.
- 该研究强调了与氧化应激相关的骨质疏松症的潜在治疗点.
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