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Genetic deletion of sonic hedgehog causes hemiagenesis and ectopic development of the thyroid in mouse.

Artikel i vetenskaplig tidskrift
Författare Henrik Fagman
Mats Grände
Amel Gritli Linde
Mikael Nilsson
Publicerad i American Journal of Pathology
Volym 164
Nummer/häfte 5
Sidor 1865-72
ISSN 0002-9440
Publiceringsår 2004
Publicerad vid Odontologiska institutionen
Institutionen för anatomi och cellbiologi
Sidor 1865-72
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Animals, Cell Differentiation, Epithelium, pathology, Gene Deletion, Hedgehog Proteins, Immunohistochemistry, In Situ Hybridization, Mice, Mice, Transgenic, RNA, Messenger, metabolism, Signal Transduction, Thyroglobulin, metabolism, Thyroid Gland, metabolism, pathology, Time Factors, Trachea, pathology, Trans-Activators, metabolism
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

Thyroid dysgenesis encountered in 85% of patients with congenital hypothyroidism is a morphologically heterogeneous condition with primarily unknown pathogenesis. Here we identify sonic hedgehog (Shh) as a novel regulator of thyroid development. In Shh knockout mice the thyroid primordium is correctly specified in the pharyngeal endoderm, but budding and dislocation are slightly delayed. In late development the thyroid fails to form a bilobed gland. Instead a single thyroid mass is found unilaterally and mostly to the left of the midline. Thyroid-specific transcription factors (TTF-1 and TTF-2) and thyroglobulin are expressed indicating terminal differentiation. Strikingly, TTF-1- and TTF-2-positive cells aberrantly develop in the presumptive trachea of Shh-/- embryos. The ectopic tissue buds ventrolaterally into the adjacent mesenchyme, and less extensively into the tracheal lumen, forming follicle-like structures that accumulate thyroglobulin. Shh mRNA is not expressed in the thyroid precursor cells at any developmental stage. The results indicate that Shh signaling indirectly governs the symmetric bilobation of the thyroid during late organogenesis. Shh also seems to repress inappropriate thyroid differentiation in nonthyroid embryonic tissues. This study provides clues to the molecular mechanisms that might be dysregulated in thyroid hemiagenesis and development of ectopic thyroid tissue outside the thyroglossal duct.

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