PUBLICATION

Myeloid cells interact with a subset of thyrocytes to promote their migration and follicle formation through NF-κB

Authors
Yang, R.M., Song, S.Y., Wu, F.Y., Yang, R.F., Shen, Y.T., Tu, P.H., Wang, Z., Zhang, J.X., Cheng, F., Gao, G.Q., Liang, J., Guo, M.M., Yang, L., Zhou, Y., Zhao, S.X., Zhan, M., Song, H.D.
ID
ZDB-PUB-231207-11
Date
2023
Source
Nature communications   14: 80828082 (Journal)
Registered Authors
Song, Huai-Dong, Zhao, Shuangxia, Zhou, Yi
Keywords
none
MeSH Terms
  • Animals
  • Mice
  • Myeloid Cells
  • NF-kappa B*
  • Thyroid Epithelial Cells*
  • Tumor Necrosis Factor-alpha
  • Zebrafish
PubMed
38057310 Full text @ Nat. Commun.
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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Human Disease / Model
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