ArticleProceedings of the National Academy of Sciences of the United States of America2012
Thyroid hormone triggers the developmental loss of axonal regenerative capacity via thyroid hormone receptor α1 and krüppel-like factor 9 in Purkinje cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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39 citing papers in PubMed, 67 citations in OpenAlex.
- Article
- Developmental neurotoxicity of thyroid hormone system-disrupting chemicals: a systems-level exploration using multi-omics approach.Archives of toxicology · 2026Article
- Endothelial Klf9 fine-tunes Akt signaling to act as a transcriptional brake restraining retinal angiogenesis.International journal of biological sciences · 2026Article
- Hepatic KLF9 Deficiency Inhibits Dehydroepiandrosterone (DHEA)-Induced Polycystic Ovary Syndrome via Liver-Ovary Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Klf9 promotes the repair of myocardial infarction by regulating macrophage recruitment and polarization.JCI insight · 2025Article
- Implications of Krüppel-like factor signaling in neuroinflammation for neurodegenerative diseases.American journal of translational research · 2025Review
- Klf9 is essential for cardiac mitochondrial homeostasis.Nature cardiovascular research · 2024Article
- Glucocorticoids increase adiposity by stimulating Krüppel-like factor 9 expression in macrophages.Nature communications · 2024Article
- Review
- International Union of Basic and Clinical Pharmacology CXIII: Nuclear Receptor Superfamily-Update 2023.Pharmacological reviews · 2023Review
- Postpartum scarcity-adversity inflicts sex-specific cerebellar adaptations and reward behaviors in adolescence.Pharmacology, biochemistry, and behavior · 2023Article
- Thyroid hormone as a temporal switch in mouse development.European thyroid journal · 2023Review
- Article
- Thyroid hormone action during GABAergic neuron maturation: The quest for mechanisms.Frontiers in endocrinology · 2023Review
- An Atlas of Thyroid Hormone Receptors' Target Genes in Mouse Tissues.International journal of molecular sciences · 2022Article
- Integrated Omic Analyses Identify Pathways and Transcriptomic Regulators Associated With Chemical Alterations of In Vitro Neural Network Formation.Toxicological sciences : an official journal of the Society of Toxicology · 2022Article
- Developmental and Injury-induced Changes in DNA Methylation in Regenerative versus Non-regenerative Regions of the Vertebrate Central Nervous System.BMC genomics · 2022Article
- Why Has the Ability to Regenerate Following CNS Injury Been Repeatedly Lost Over the Course of Evolution?Frontiers in neuroscience · 2022Article
- Article
- Accelerated cell cycles enable organ regeneration under developmental time constraints in the Drosophila hindgut.Developmental cell · 2021Article
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Authors and funding
11 authors at 7 institutions in 3 countries.
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Abstract
Neurons in the CNS of higher vertebrates lose their ability to regenerate their axons at a stage of development that coincides with peak circulating thyroid hormone (T(3)) levels. Here, we examined whether this peak in T(3) is involved in the loss of axonal regenerative capacity in Purkinje cells (PCs). This event occurs at the end of the first postnatal week in mice. Using organotypic culture, we found that the loss of axon regenerative capacity was triggered prematurely by early exposure of mouse PCs to T(3), whereas it was delayed in the absence of T(3). Analysis of mutant mice showed that this effect was mainly mediated by the T(3) receptor α1. Using gain- and loss-of-function approaches, we also showed that Krüppel-like factor 9 was a key mediator of this effect of T(3). These results indicate that the sudden physiological increase in T(3) during development is involved in the onset of the loss of axon regenerative capacity in PCs. This loss of regenerative capacity might be part of the general program triggered by T(3) throughout the body, which adapts the animal to its postnatal environment.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.