Shen Jianlin, Zhang Qiang, Lan Yujian, Peng Qingping, Ji Ziyu, Wu Yanjiao, Liu Huan
Department of Orthopaedics, Affiliated Hospital of Putian University, 351100 Putian, Fujian, China.
Central Laboratory, Affiliated Hospital of Putian University, 351100 Putian, Fujian, China.
Front Biosci (Landmark Ed). 2024 Nov 28;29(12):405. doi: 10.31083/j.fbl2912405.
The mechanism for RNA methylation during disc degeneration is unclear. The aim of this study was to identify N6-methyladenosine (m6A) markers and therapeutic targets for the prevention and treatment of intervertebral disc degeneration (IDD).
Methylated RNA immunoprecipitation sequencing (MeRIP-seq) and quantitative reverse transcription PCR (RT-qPCR) were employed to analyze m6A modifications of IDD-related gene expression. Bioinformatics was used to identify enriched gene pathways in IDD. m6A-RIP-qPCR was used to validate potential targets and markers.
Human IDD samples exhibited a distinct m6A modification pattern that allowed associated genes and pathways to be identified. These genes had functions such as "nuclear factor kappa-B (NF-κB) binding" and "extracellular matrix components", which are crucial for IDD pathogenesis. showed increased m6A modification in IDD, while and showed decreased m6A methylation. The results of this study offer novel insights for the prevention and treatment of IDD.
椎间盘退变过程中RNA甲基化的机制尚不清楚。本研究旨在鉴定N6-甲基腺苷（m6A）标记物及预防和治疗椎间盘退变（IDD）的治疗靶点。
采用甲基化RNA免疫沉淀测序（MeRIP-seq）和定量逆转录PCR（RT-qPCR）分析IDD相关基因表达的m6A修饰。利用生物信息学鉴定IDD中富集的基因通路。m6A-RIP-qPCR用于验证潜在靶点和标记物。
人类IDD样本呈现出独特的m6A修饰模式，据此可鉴定相关基因和通路。这些基因具有“核因子κB（NF-κB）结合”和“细胞外基质成分”等功能，对IDD发病机制至关重要。[具体基因名称]在IDD中m6A修饰增加，而[具体基因名称]和[具体基因名称]的m6A甲基化减少。本研究结果为IDD的预防和治疗提供了新的见解。
