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Expression of Classical Cadherins in Thyroid Development: Maintenance of an Epithelial Phenotype throughout Organogenesis

Institute of Anatomy and Cell Biology (H.F., M.G., M.N.) and Department of Medical Biochemistry (J.E., H.S.), Goteborg University, SE-40530 Goteborg, Sweden

Address all correspondence and requests for reprints to: Dr. Henrik Fagman, Institute of Anatomy and Cell Biology, Goteborg University, Box 420, SE-40530 Goteborg, Sweden. E-mail: henrik.fagman{at}anatcell.gu.se.

The long distance between the final location of the thyroid gland in front of the trachea and the site of embryological specification at the tongue base suggests that active migration of the thyroid progenitor cells is required. During embryogenesis, similar morphogenetic events often involve epithelial to mesenchymal transition (EMT), which promotes the acquisition of a migrating phenotype. EMT is characterized by an altered expression of cadherin cell adhesion molecules, most notably loss of E-cadherin. To investigate whether a similar mechanism operates in thyroid development, we studied the expression of classical cadherins in the thyroid primordium of mouse embryos by immunohistochemistry. E-Cadherin was expressed at high levels in thyroid cells at all developmental stages. In contrast, R-cadherin expression was induced in the embryonic thyroid coinciding with the onset of folliculogenesis and was maintained in the adult thyroid along with E-cadherin. N-Cadherin, often associated with increased migrating capacity, was not detected in the thyroid primordium, but was expressed in the surrounding mesenchyme. These findings indicate that the epithelial phenotype is maintained in thyroid progenitor cells throughout organogenesis and favor the idea that translocation of the developing thyroid does not involve active migration of individual cells, but rather is secondary to movements of surrounding tissues.

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