| First Author | Yang RM | Year | 2023 |
| Journal | Nat Commun | Volume | 14 |
| Issue | 1 | Pages | 8082 |
| PubMed ID | 38057310 | Mgi Jnum | J:357240 |
| Mgi Id | MGI:7564823 | Doi | 10.1038/s41467-023-43895-8 |
| Citation | Yang RM, et al. (2023) Myeloid cells interact with a subset of thyrocytes to promote their migration and follicle formation through NF-kappaB. Nat Commun 14(1):8082 |
| abstractText | 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-kappaB-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-kappaB 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-alpha. 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-alpha-induced NF-kappaB activation plays a critical role in promoting the migration of vertebrate thyrocytes for follicle generation. |
