ArticleJournal of endocrinological investigation2024
Mouse model of Graves' orbitopathy induced by the immunization with TSHR A and IGF-1R α subunit gene.
Article in Journal of endocrinological investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 4 citations in OpenAlex.
- A bispecific-aptamer TSHR-CD80-1 treats thyroid eye disease by inhibiting CD8Cell communication and signaling : CCS · 2026Article
- Mouse Model of Graves' Orbitopathy in Current Research and Future Perspectives.Medicina (Kaunas, Lithuania) · 2026Review
- Unravelling the pathogenic mechanisms in Graves' orbitopathy.European thyroid journal · 2025Review
- Specific molecular imaging of BALB/c model mice with Graves' ophthalmopathy based on high expression of insulin-like growth factor 1 receptor.Annals of nuclear medicine · 2025Article
- Molecular Mechanism of Microgravity-Induced Intestinal Flora Dysbiosis on the Abnormalities of Liver and Brain Metabolism.International journal of molecular sciences · 2025Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
purposeThe study aimed to establish a mouse model of Graves' disease (GD) with Graves' orbitopathy (GO; GD + GO) that can represent the clinical disease characteristics.
methodsA eukaryotic expression plasmid of insulin-like growth factor 1 receptor (IGF-1R) α subunit (pcDNA3.1/IGF-1Rα) and a thyrotropin receptor (TSHR) A subunit plasmid (pcDNA3.1/TSHR-289) were injected in female BALB/c mice followed by immediate electroporation to induce a GD + GO model. Grouping was performed according to the frequency of injection (2- to 4-week intervals) and type of injected plasmids: T: pcDNA3.1/TSHR-289( +), I: pcDNA3.1/IGF-1Rα( +), or co-injection T + I: pcDNA3.1/TSHR-289( +) and pcDNA3.1/IGF-1Rα( +). Serum TSH, T4, TSAb, TSBAb, body weight, and blood glucose levels were evaluated. Thyroid
resultsA total of 60% of mice (3/5, one mouse died) in the T group developed GD + GO. In the T + I group, 83.3% of mice (5/6) developed GD + GO. Mice in the I group did not develop GD. Compared with the control group, serum T4, TSAb, and TSBAb of the mice in the GD + GO model groups were increased to varying degrees (P < 0.05), and serum TSH and body weight were significantly lower compared to the control group (P < 0.05). The thyroid uptake capacity of
conclusionsWe successfully induced a GD + GO mouse model by a repeated co-injection of pcDNA3.1/IGF-1Rα and pcDNA3.1/TSHR-289 plasmids. Injection of pcDNA3.1/IGF-1Rα alone failed to induce GD. Co-injection of two plasmids induced more severe GD + GO than pcDNA3.1/TSHR-289( +) alone.
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