Yu Hong, Li Zuoxi, Gao Xiao, Liu Xuehuan, Cui Weiwei, Li Ningjun, Lian Xinying, Li Can, Liu Jun
Tianjin Fourth Central Hospital, The Affiliated Hospital of Tianjin Medical University, Tianjin 300140, China.
Department of Radiology, Tianjin Union Medical Center, Tianjin 300121, China.
Prog Neuropsychopharmacol Biol Psychiatry. 2025 Jan 10;136:111239. doi: 10.1016/j.pnpbp.2024.111239. Epub 2024 Dec 28.
The mechanisms underlying the complex relationship between autoimmune hypothyroidism and neurological disorders remain unclear. We conducted a comprehensive analysis of associations between alternative splicing, transcriptomics, and proteomics data and autoimmune hypothyroidism.
Splicing-wide association studies (SWAS), proteome-wide association studies (PWAS), and transcriptome-wide association studies (TWAS) were used to identify genes and proteins that regulate autoimmune hypothyroidism within the brain axis. We performed TWAS on GTEx V8 thyroid tissue data to identify autoimmune hypothyroidism-associated thyroid axis genes. A FUSION analysis of overlapping genes in the brain and thyroid axes and brain splicing weights was conducted to determine the influence of alternative splicing in the brain on thyroid tissue gene expression.
SWAS identified 223 alternative splicing events, TWAS identified 270 genes, and PWAS revealed five genes (FDPS, PPIL3, PEX6, MMAB, and ALDH2) encoding proteins associated with autoimmune hypothyroidism. Neuroimaging analyses revealed distinct brain-imaging phenotypes associated with these five genes. TWAS of thyroid tissue identified four genes (FDPS, PPIL3, MMAB, and ALDH2) associated with the brain axis related to thyroid tissue. A FUSION analysis indicated that alternative splicing changes in ALDH2 in brain tissue influenced its expression in thyroid tissue.
Integrating brain splicing, proteomic, and transcriptomic data supports the association between specific genes and proteins in the brain and autoimmune hypothyroidism. Additionally, ALDH2 alternative splicing in brain tissue influences its thyroid tissue expression. These findings provide new insights into the molecular basis of autoimmune hypothyroidism, facilitating future pathogenesis research.
自身免疫性甲状腺功能减退症与神经系统疾病之间复杂关系的潜在机制仍不清楚。我们对可变剪接、转录组学和蛋白质组学数据与自身免疫性甲状腺功能减退症之间的关联进行了全面分析。
使用全剪接关联研究(SWAS)、全蛋白质组关联研究(PWAS)和全转录组关联研究(TWAS)来识别在脑轴内调节自身免疫性甲状腺功能减退症的基因和蛋白质。我们对GTEx V8甲状腺组织数据进行TWAS,以识别与自身免疫性甲状腺功能减退症相关的甲状腺轴基因。对脑轴和甲状腺轴中的重叠基因以及脑剪接权重进行FUSION分析,以确定脑中可变剪接对甲状腺组织基因表达的影响。
SWAS识别出223个可变剪接事件,TWAS识别出270个基因,PWAS揭示了五个编码与自身免疫性甲状腺功能减退症相关蛋白质的基因(FDPS、PPIL3、PEX6、MMAB和ALDH2)。神经影像学分析揭示了与这五个基因相关的独特脑成像表型。甲状腺组织的TWAS识别出四个与甲状腺组织相关脑轴的基因(FDPS、PPIL3、MMAB和ALDH2)。FUSION分析表明,脑组织中ALDH2的可变剪接变化影响其在甲状腺组织中的表达。
整合脑剪接、蛋白质组学和转录组学数据支持脑中特定基因和蛋白质与自身免疫性甲状腺功能减退症之间的关联。此外,脑组织中ALDH2的可变剪接影响其在甲状腺组织中的表达。这些发现为自身免疫性甲状腺功能减退症的分子基础提供了新见解,有助于未来发病机制的研究。