ArticleMolecular endocrinology (Baltimore, Md.)2011
TSH compensates thyroid-specific IGF-I receptor knockout and causes papillary thyroid hyperplasia.
Article in Molecular endocrinology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Polystyrene Microplastics-Induced Thyroid Dysfunction in Mice: A Study of Gene Expression, Oxidative Stress, and Histopathological Changes.Veterinary medicine and science · 2025Article
- Teprotumumab in the management of thyroid eye disease mechanistic insights and adverse reactions: a comprehensive review.Frontiers in endocrinology · 2025Review
- Defining theThyroid : official journal of the American Thyroid Association · 2024Article
- Functional variants in a TTTG microsatellite on 15q26.1 cause familial nonautoimmune thyroid abnormalities.Nature genetics · 2024Article
- Mice with gene alterations in the GH and IGF family.Pituitary · 2022Review
- Connecting the Dots Between the Gut-IGF-1-Prostate Axis: A Role of IGF-1 in Prostate Carcinogenesis.Frontiers in endocrinology · 2022Review
- Epigenetic modification and BRAF gene mutation in thyroid carcinoma.Cancer cell international · 2021Review
- Article
- AATF and SMARCA2 are associated with thyroid volume in Hashimoto's thyroiditis patients.Scientific reports · 2020Article
- Insulin-like Growth Factor-I Receptor and Thyroid-Associated Ophthalmopathy.Endocrine reviews · 2019Review
- Thyrocyte-specific deletion of insulin and IGF-1 receptors induces papillary thyroid carcinoma-like lesions through EGFR pathway activation.International journal of cancer · 2018Article
- 40 YEARS of IGF1: Understanding the tissue-specific roles of IGF1/IGF1R in regulating metabolism using the Cre/loxP system.Journal of molecular endocrinology · 2018Review
- [Genetics of thyroid nodules and thyroid carcinoma].Der Internist · 2018Review
- Involvement of Igf1r in Bronchiolar Epithelial Regeneration: Role during Repair Kinetics after Selective Club Cell Ablation.PloS one · 2016Article
- Disrupted TSH Receptor Expression in Female Mouse Lung Fibroblasts Alters Subcellular IGF-1 Receptor Distribution.Endocrinology · 2015Article
- Differential organ phenotypes after postnatal Igf1r gene conditional deletion induced by tamoxifen in UBC-CreERT2; Igf1r fl/fl double transgenic mice.Transgenic research · 2015Article
- The Novel Functions of High-Molecular-Mass Complexes Containing Insulin Receptor Substrates in Mediation and Modulation of Insulin-Like Activities: Emerging Concept of Diverse Functions by IRS-Associated Proteins.Frontiers in endocrinology · 2015Review
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although TSH stimulates all aspects of thyroid physiology IGF-I signaling through a tyrosine kinase-containing transmembrane receptor exhibits a permissive impact on TSH action. To better understand the importance of the IGF-I receptor in the thyroid in vivo, we inactivated the Igf1r with a Tg promoter-driven Cre-lox system in mice. We studied male and female mice with thyroidal wild-type, Igf1r(+/-), and Igf1r(-/-) genotypes. Targeted Igf1r inactivation did transiently reduce thyroid hormone levels and significantly increased TSH levels in both heterozygous and homozygous mice without affecting thyroid weight. Histological analysis of thyroid tissue with Igf1r inactivation revealed hyperplasia and heterogeneous follicle structure. From 4 months of age, we detected papillary thyroid architecture in heterozygous and homozygous mice. We also noted increased body weight of male mice with a homozygous thyroidal null mutation in the Igf1r locus, compared with wild-type mice, respectively. A decrease of mRNA and protein for thyroid peroxidase and increased mRNA and protein for IGF-II receptor but no significant mRNA changes for the insulin receptor, the TSH receptor, and the sodium-iodide-symporter in both Igf1r(+/-) and Igf1r(-/-) mice were detected. Our results suggest that the strong increase of TSH benefits papillary thyroid hyperplasia and completely compensates the loss of IGF-I receptor signaling at the level of thyroid hormones without significant increase in thyroid weight. This could indicate that the IGF-I receptor signaling is less essential for thyroid hormone synthesis but maintains homeostasis and normal thyroid morphogenesis.
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