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Corrigendum Free access | 10.1172/JCI80031

Embryonic exposure to excess thyroid hormone causes thyrotrope cell death

Ksenia N. Tonyushkina, Meng-Chieh Shen, Theresa Ortiz-Toro, and Rolf O. Karlstrom

Find articles by Tonyushkina, K. in: JCI | PubMed | Google Scholar

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Published February 2, 2015 - More info

Published in Volume 125, Issue 2 on February 2, 2015
J Clin Invest. 2015;125(2):881–881. https://doi.org/10.1172/JCI80031.
Copyright © 2015, American Society for Clinical Investigation
Published February 2, 2015 - Version history
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Related article:

Embryonic exposure to excess thyroid hormone causes thyrotrope cell death
Ksenia N. Tonyushkina, … , Theresa Ortiz-Toro, Rolf O. Karlstrom
Ksenia N. Tonyushkina, … , Theresa Ortiz-Toro, Rolf O. Karlstrom
Research Article

Embryonic exposure to excess thyroid hormone causes thyrotrope cell death

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Abstract

Central congenital hypothyroidism (CCH) is more prevalent in children born to women with hyperthyroidism during pregnancy, suggesting a role for thyroid hormone (TH) in the development of central thyroid regulation. Using the zebrafish embryo as a model for thyroid axis development, we have characterized the ontogeny of negative feedback regulation of thyrotrope function and examined the effect of excess TH on thyrotrope development. We found that thyroid-stimulating hormone β subunit (tshb) and type 2 deiodinase (dio2) are coexpressed in zebrafish thyrotropes by 48 hours after fertilization and that TH-driven negative feedback regulation of tshb transcription appears in the thyroid axis by 96 hours after fertilization. Negative feedback regulation correlated with increased systemic TH levels from the developing thyroid follicles. We used a transgenic zebrafish that expresses GFP under the control of the tshb promoter to follow thyrotrope fates in vivo. Time-lapse imaging revealed that early exposure to elevated TH leads to thyrotrope cell death. Thyrotrope numbers slowly recovered following the removal of excess TH. These data demonstrate that transient TH exposure profoundly impacts the thyrotrope population during a critical period of pituitary development and may have long-term implications for the functional reserve of thyroid-stimulating hormone (TSH) production and the TSH set point later in life.

Authors

Ksenia N. Tonyushkina, Meng-Chieh Shen, Theresa Ortiz-Toro, Rolf O. Karlstrom

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Original citation: J Clin Invest. 2014;124(1):321–327. doi:10.1172/JCI70038.

Citation for this corrigendum: J Clin Invest. 2015;125(2):881. doi:10.1172/JCI80031.

An incorrect e-mail address was given for corresponding author Rolf Karlstrom. The correct address is below.

karlstrom@bio.umass.edu

The authors regret the error.

Footnotes

See the related article beginning on page 321.

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