ISSN 1662-4009 (Online)

ESPE Yearbook of Paediatric Endocrinology (2019) 16 3.1 | DOI: 10.1530/ey.16.3.1

Primary cilium in the human thyrocyte: changes in frequency and length in relation to the functional pathology of the thyroid gland

Fernández-Santos JM, Utrilla JC, Vázquez-Román V, Villar-Rodríguez JL, Gutiérrez-Avilés L & Martín-Lacave I

To read the full abstract: Thyroid. 2019;29:595–606.

Here, ultrastructural analysis of primary cilia in human thyroid follicles revealed a direct relationship between frequency and length of primary cilia and the functional state of the individual follicle in normal compared to hyperfunctioning thyroid tissues.

Primary cilia are present in many different tissues. They are involved in key processes of cell physiology during development and homeostasis, e.g. mediating intraocular pressure sensation. Human diseases associated with defective cilia function are called ciliopathies, affecting a broad range of organs such as eye, brain, kidney, liver, and many more, reviewed in detail by Reiter and Leroux [1]. Although primary cilia in the human thyroid have been described decades ago, their putative role for the angio-follicular unit of the thyroid has not been investigated so far. This study provides a detailed morphometric and electron microcopy study of normal thyroid tissues compared to nodular hyperplasia and Graves’ disease tissues to describe quantitatively the changes of primary cilia in different conditions of thyroid activity.

The key result was that the number and length of primary cilia was significantly negatively associated with the functional level of the thyroid tissues. Analyzing >1300 thyroid follicles and 43,000 thyrocytes, they showed lower number and shorter cilia length in hyperfunctioning tissues (nodular hyperplasia and Graves’ disease) in contrast to normal thyroid tissues. The authors hypothesize that in analogy with other organs, where cilia have sensing functions for key physiological processes, thyroid follicular cell cilia might be involved in intrafollicular sensing of iodinated thyroglobulin and could have regulatory function for thyroid hormonogenesis for the thyrocyte. Recent work in the mouse model provide first molecular evidence for such regulatory mechanisms [2]. The question arises whether defects in thyroidal ciliogenesis could cause genetic hypothyroidism.

References: 1. Reiter JF, Leroux MR. Genes and molecular pathways underpinning ciliopathies. Nat Rev Mol Cell Biol 2017;18:533–47.

2. Qatato M, Szumska J, Skripnik V, Rijntjes E, Köhrle J, Brix K. Canonical TSH regulation of cathepsin-mediated thyroglobulin processing in the thyroid gland of male mice requires Taar1 expression. Front Pharmacol. 2018;9:221.PMID: 29615904.

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