ETA2022 Poster Presentations Thyroid Hormone Transporters and Development (8 abstracts)
Transcriptomic signature of human embryonic thyroid reveals transition from differentiation to functional maturation
Geneviève Dom 1 , Petr Dmitriev 1 , Marie-Alexandra Lambot 2 , Guy Van Vliet 3 , Daniel Glinoer 4 , Frederick Libert 5 , Anne Lefort 1 , Jacques E. Dumont 1 & Carine Maenhaut 1
1Université Libre de Bruxelles, Faculté de Médecine, Iribhm, Brussels, Belgium; 2Hôpital Saint-Pierre, Universté Libre de Bruxelles, Brussels, Belgium; 3Université de Montréal, Département de Pédiatrie, Canada; 4Hôpital Saint-Pierre, Université Libre de Bruxelles, Brussels, Belgium; 5Université Libre de Bruxelles, Iridia, Brussels, Belgium
The human thyroid gland acquires a differentiation program as early as weeks 3–4 of embryonic development. The onset of functional differentiation, which manifests by the appearance of colloid in thyroid follicles, takes place during gestation weeks10–11. By 12–13 weeks functional differentiation is accomplished and the thyroid is capable of producing thyroid hormones although at a low level. During maturation, thyroid hormones yield increases and physiological mechanisms of thyroid hormone synthesis regulation are established. In the present work we traced the process of thyroid functional differentiation and maturation in the course of human development by performing transcriptomic analysis of human thyroids covering the period of gestation weeks 7–11 and comparing it to adult human thyroid. We obtained specific transcriptomic signatures of embryonic and adult human thyroids by comparing them to non-thyroid tissues from human embryos and adults. Remarkable upregulations of signaling growth factors such as IGF1 and FGF, already found to be involved in animal models of thyroid development, as well proteins involved in the cAMP pathway regulation and activity were highlighted in this transcriptomic analysis of human fetal/embryonic thyroids. This gives clues to explain how this pathway, crucial for the differentiation of thyroid cells, is activated in the absence of TSH during embryonic/fetal development. We defined a non-TSH (thyroid stimulating hormone) dependent transition from differentiation to maturation of thyroid. The study also sought to shed light on possible factors that could replace TSH, which is absent in this window of gestational age, to trigger transition to the emergence of thyroid function. We propose a list of possible genes that may also be involved in abnormalities in thyroid differentiation and/or maturation, hence leading to congenital hypothyroidism.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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