ArticleHeliyon2024
Peptidomic profiling of endogenous peptides in the spleens of mouse models of Graves' disease.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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3 authors.
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Abstract
Background: Graves' disease (GD) is a common autoimmune thyroid disorder. The pathogenesis of GD involves an autoimmune response to the A subunit of the human thyrotropin receptor (hTSHR), although the specific mechanisms are not fully elucidated. Methods: This study established a GD model by immunizing BALB/c mice with a recombinant adenovirus expressing the hTSHR A subunit. Spleen tissues were collected and analyzed using liquid chromatography-tandem mass spectrometry (LC-MS/MS) to identify differentially expressed peptides (DEPs). Gene Ontology (GO) analysis and KEGG pathway analysis were further utilized to annotate the functions of these DEPs. Additionally, peptide bioactivity prediction and molecular docking studies were conducted using Alphafold and Pymol software, respectively, to assess the binding affinity of specific peptides to the hTSHR A subunit. Results: The GD mouse model was successfully established, and 1,428 DEPs were identified in the spleen, with 368 upregulated and 1,060 downregulated. Functional analysis indicated that these DEPs are mainly involved in cellular endocytosis, regulation of gene expression, and nucleocytoplasmic transport. Notably, molecular docking studies revealed that the abnormally highly expressed peptide HG2A-24aa demonstrated potential bioactivity and strong binding affinity with hTSHR-289aa. Conclusion: The specific bioactive peptides may play key roles in the pathogenesis of GD, particularly HG2A-24aa, which may have a significant role in the MHC II antigen presentation pathway mediated by the hTSHR A subunit.
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