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Synthesis and Regulation of Thyroid Hormones

Synthesis and Regulation of Thyroid Hormones

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.
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The...

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An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma

Published on: April 17, 2013

PAPP-A as a Potential Target in Thyroid Eye Disease.

Cheryl A Conover¹, Laurie K Bale¹, Marius N Stan¹

¹Division of Endocrinology, Mayo Clinic, Rochester, MN 55905, USA.

The Journal of Clinical Endocrinology and Metabolism

|May 16, 2024

Summary

Targeting PAPP-A, an enzyme involved in thyroid eye disease (TED), may offer a new therapeutic approach. Inhibiting PAPP-A reduces IGF-IR signaling, potentially treating proptosis and visual dysfunction in TED patients.

Keywords:

PAPP-A fibrocytes insulin-like growth factor proinflammatory cytokines thyroid eye disease

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Area of Science:

Ophthalmology
Endocrinology
Molecular Biology

Background:

Thyroid eye disease (TED) can cause proptosis, leading to disfigurement and vision loss.
Current treatments for proptosis, like IGF-IR inhibitors, are effective but have side effects.

Purpose of the Study:

To investigate if PAPP-A inhibitors can selectively reduce IGF-IR signaling in TED.
To assess the role of PAPP-A in the pathogenesis of TED.

Main Methods:

TED fibroblasts were cultured and treated with proinflammatory cytokines.
Fibroblasts were separated into CD34- and CD34+ populations.
PAPP-A expression, proteolytic activity, and IGF-IR signaling were measured.

Main Results:

Cytokines increased PAPP-A expression in TED fibroblasts.
Inhibiting PAPP-A suppressed IGF-IR activation.
CD34+ fibroblasts were the primary source of PAPP-A and IGF-IR.

Conclusions:

PAPP-A plays a significant role in TED.
Targeting PAPP-A offers a potential new therapeutic strategy for TED.