ArticleNature communications2023
Myeloid cells interact with a subset of thyrocytes to promote their migration and follicle formation through NF-κB.
Article in Nature communications, 2023. 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.
- Resolving thyroid lineage cell trajectories merging into a dual endocrine gland in mammals.Nature communications · 2026Article
- Tead1a Initiates Transcriptional Priming Through the TEAD1a/YAP-Notch1-Spi1/Cebpα Axis to Promote Neutrophil Fate.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Oligomeric hyaluronic acid-modified liposomes effectively improved skin permeability and anti-ageing activity of ellagic acid.Scientific reports · 2025Article
- Androgen receptor deficiency-induced TUG1 in suppressing ferroptosis to promote benign prostatic hyperplasia through the miR-188-3p/GPX4 signal pathway.Redox biology · 2024Article
- Deficiency of the HGF/Met pathway leads to thyroid dysgenesis by impeding late thyroid expansion.Nature communications · 2024Article
Corrections and comments
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Authors and funding
17 authors at 7 institutions in 2 countries.
Funding
Abstract
The pathogenesis of thyroid dysgenesis (TD) is not well understood. Here, using a combination of single-cell RNA and spatial transcriptome sequencing, we identify a subgroup of NF-κB-activated thyrocytes located at the center of thyroid tissues in postnatal mice, which maintained a partially mesenchymal phenotype. These cells actively protruded out of the thyroid primordium and generated new follicles in zebrafish embryos through continuous tracing. Suppressing NF-κB signaling affected thyrocyte migration and follicle formation, leading to a TD-like phenotype in both mice and zebrafish. Interestingly, during thyroid folliculogenesis, myeloid cells played a crucial role in promoting thyrocyte migration by maintaining close contact and secreting TNF-α. We found that cebpa mutant zebrafish, in which all myeloid cells were depleted, exhibited thyrocyte migration defects. Taken together, our results suggest that myeloid-derived TNF-α-induced NF-κB activation plays a critical role in promoting the migration of vertebrate thyrocytes for follicle generation.
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Registered trials
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