AsianScientist (May 25, 2017) – In a study published in EMBO Molecular Medicine, researchers have found out how the thyroid changes in patients with Graves’ disease. Their findings provide a potential therapeutic target for thyroid diseases.
The thyroid is a highly vascularized organ found behind the Adam’s apple. Some of the functions of the thyroid are regulated by a hormone called thyrotropin, produced in the brain. Graves’ disease, the most common cause of hyperthyroidism in the United States, affects both the thyroid and the surrounding vascular network. In this disease, the thyroid produces an excessive amount of hormones and the capillaries become denser.
“Previous studies show that abnormalities in thyroid glands and surrounding vasculature are interconnected, we wanted to understand how this happens at the molecular level,” explained team leader Koh Gou Young, director of the Center for Vascular Research within the Institute for Basic Science (IBS).
Using animal models that simulate Graves’ disease, Koh’s team uncovered a biological pathway contributing to this disorder. They found that the culprit is the vascular endothelial growth factor A (VEGF-A). This protein is involved in forming new vessels around the thyroid, and regulating the hormonal exchange happening between these vessels and the thyroid, through very small pores called fenestrae (from Latin ‘window’).
Upon stimulation with the thyrotropin hormone, VEGF-A is produced by the thyroid gland, causing the thyroid to enlarge and turning on the expression of the VEGF-A receptor, VEGFR2, in the walls of the surrounding capilliaries. By blocking VEGFR2, the scientists could inhibit enlargement of the thyroid and stop vascular remodeling.
“Our findings identify VEGFR2 blockade as a novel therapeutic avenue for targeting thyroid disease associated with thyrotropin,” explained Koh.
The researchers also found that the angiopoietin-Tie2 pathway, fundamental in other tissues like the eyes and brain, does not play a major role in remodeling the vasculature of the thyroid gland. Finally, they rules out VEGFR3 as a protein essential for thyroid vascular integrity.
Source: Institute for Basic Science.
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