Mostaghimi Yasaman, Haddadi Mohammad, Hojjati Zohreh
Department of Biology, Faculty of Basic Sciences, University of Zabol, Zabol, Iran.
Department of Biology, Faculty of Sciences, University of Isfahan, Isfahan, Iran.
J Mol Neurosci. 2025 Apr 14;75(2):49. doi: 10.1007/s12031-025-02331-w.
Multiple sclerosis (MS), an autoimmune condition of the central nervous system (CNS), can lead to demyelination and axonal degeneration in the brain and spinal cord, which can cause progressive neurologic disability. MS symptoms include dysautonomia and progressive decline in motor abilities. In this investigation, we performed an integrated bioinformatics and experimental approach to find the expression level and interaction of a novel long non-coding RNA (lncRNA), PAN3-AS1, in MS samples. Microarray analysis was performed by R Studio using GEOquery and limma packages. lncRNA-mRNA RNA interaction analysis was performed using the lncRRIsearch database. Pathway enrichment analysis was performed by KEGG and Reactome online software through the Enrichr database. Protein-protein interaction analysis was performed by STRING online software. Gene ontology (GO) analysis was performed by Enrichr database. Based on microarray analysis, lncRNA PAN3-AS1 has a significantly low expression in MS samples compared to the control (logFC - 1.2, adj. P. Val 0.03). qRT-PCR results approved bioinformatics analyses. ROC analysis revealed that PAN3-AS1 could be considered a potential diagnostic biomarker of MS. Based on lncRNA-mRNA interaction analysis, lncRNA PAN3-AS1 regulates the expression level of RPGR. RPGR and its protein interactome regulate the cilium assembly, chaperon-mediated autophagy, and microarray biogenesis. lncRNA PAN3-AS1, as a significant low-expressed lncRNA in MS samples, could be a potential diagnostic MS biomarker. PAN3-AS1 might regulate the expression level of cilium assembly and chaperon-mediated autophagy. Dysregulation of PAN3-AS1 might affect the expression of RPGR and its protein interactome.
多发性硬化症(MS)是一种中枢神经系统(CNS)的自身免疫性疾病,可导致大脑和脊髓的脱髓鞘和轴突退化,进而引起进行性神经功能障碍。MS症状包括自主神经功能障碍和运动能力的逐渐下降。在本研究中,我们采用综合生物信息学和实验方法,以探究一种新型长链非编码RNA(lncRNA)PAN3-AS1在MS样本中的表达水平及其相互作用。使用R Studio通过GEOquery和limma软件包进行微阵列分析。使用lncRRIsearch数据库进行lncRNA-mRNA RNA相互作用分析。通过KEGG和Reactome在线软件经Enrichr数据库进行通路富集分析。使用STRING在线软件进行蛋白质-蛋白质相互作用分析。通过Enrichr数据库进行基因本体(GO)分析。基于微阵列分析,与对照组相比,lncRNA PAN3-AS1在MS样本中的表达显著降低(logFC -1.2,校正P值0.03)。qRT-PCR结果证实了生物信息学分析。ROC分析表明,PAN3-AS1可被视为MS的潜在诊断生物标志物。基于lncRNA-mRNA相互作用分析,lncRNA PAN3-AS1调节RPGR的表达水平。RPGR及其蛋白质相互作用组调节纤毛组装、伴侣介导的自噬和微阵列生物发生。lncRNA PAN3-AS1作为MS样本中显著低表达的lncRNA,可能是MS的潜在诊断生物标志物。PAN3-AS1可能调节纤毛组装和伴侣介导的自噬的表达水平。PAN3-AS1的失调可能影响RPGR及其蛋白质相互作用组的表达。