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Synthesis and Regulation of Thyroid Hormones

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Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
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The thyroid hormone (TH) plays a pivotal role in the intricate orchestration of physiological processes, exerting profound effects on development, metabolism, and homeostasis throughout different life stages.
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Related Experiment Video

Updated: May 9, 2026

Functional Characterization of Endogenously Expressed Human RYR1 Variants

Functional Characterization of Endogenously Expressed Human RYR1 Variants

Published on: June 9, 2021

Ca(2+)-binding protein expression in primary human thyrocytes.

S Lorenz¹, G Aust², K Krohn³

¹Department for Internal Medicine, Clinic for Endocrinology and Nephrology, Faculty of Medicine, University of Leipzig, D-04103 Leipzig, Germany; Interdisciplinary Center for Clinical Research, Faculty of Medicine, University of Leipzig, D-04103 Leipzig, Germany.

Biochimica Et Biophysica Acta

|July 27, 2013

Summary

This summary is machine-generated.

Thyroid-stimulating hormone (TSH) fine-tunes calcium signals in human thyrocytes by regulating calcium-binding proteins (CaBP). This novel mechanism impacts thyroid cell signaling and function.

Keywords:

AFTN Annexin CTN CaBP Calcium-binding protein PHT S100 protein ST Thyroid cancer Thyroid physiology Thyroid signal transduction autonomously functioning thyroid nodule calcium binding protein cold benign thyroid nodule primary human thyrocytes surrounding tissue

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Measuring Nucleotide Binding to Intact, Functional Membrane Proteins in Real Time

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Published on: March 11, 2021

Area of Science:

Endocrinology
Molecular Biology
Cell Signaling

Background:

Calcium-binding proteins (CaBP) from S100 and annexin families are regulated by TSH in FRTL-5 cells.
Investigating CaBP regulation in primary human thyrocytes (PHT) from different thyroid tissues is crucial for understanding thyroid physiology.

Purpose of the Study:

To study the regulation of S100A4, S100A6, and ANXA2 in PHT.
To investigate the effect of CaBP expression on calcium (Ca2+) and TSH receptor (TSHR) signaling.
To explore the role of CaBP in thyroid cell proliferation and differentiation.

Main Methods:

Assessed CaBP expression (S100A4, S100A6, ANXA2) in PHT from surrounding tissues, cold benign thyroid nodules, and autonomously functioning thyroid nodules.
Utilized cell culture models accounting for PHT proliferation and differentiation markers (FOS, TPO).
Investigated signaling pathways (PKA, MEK1/2, PI3-K) and triiodothyronine involvement in CaBP regulation.
Analyzed Ca2+ signaling responses to ATP and TSH.
Employed S100A4 mutants to study protein interaction effects.

Main Results:

CaBP regulation strongly correlated with the proliferation marker FOS.
PKA, MEK1/2, PI3-K, and triiodothyronine were identified as regulators of CaBP expression.
Modulated CaBP expression altered ATP-elicited Ca2+ signaling; S100A4 affected subsequent Ca2+ responses and buffering, while ANXA2 influenced the initial Ca2+ response.
S100A4 overexpression reduced TSH-induced NFAT activation.
S100A4's effects on Ca2+ signaling are mediated by protein interactions.

Conclusions:

TSH regulates CaBP expression, thereby fine-tuning Ca2+ signals in thyrocytes.
This represents a novel cross-regulating mechanism in thyrocytes with potential implications for thyroid cell signaling and physiology.
CaBP play distinct roles in modulating Ca2+ signaling dynamics within thyroid cells.