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A culprit of thyroid's diseases

Date:
May 18, 2017
Source:
Institute for Basic Science
Summary:
A team of scientists has clarified the molecular mechanism to explain how the thyroid and surrounding vascular system change in the most common form of hyperthyroidism. These findings provide a potential therapeutic target for thyroid diseases.
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A team led by KOH Gou Young, director of the Center for Vascular Research, within the Institute for Basic Science (IBS), in collaboration with Chungnam National University, clarified the molecular mechanism to explain how the thyroid and surrounding vascular system change in the most common form of hyperthyroidism. Published in the EMBO Molecular Medicine journal, these 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," explains Koh.

Using animal models that simulate Graves' disease, IBS scientists uncovered the 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 and as a result, the thyroid enlarges and the walls of the capillaries (constituted mainly by endothelial cells) increase the expression of VEGFR2, the receptor for VEGF-A.

By blocking VEGFR2, IBS 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," explains Koh.

Concurrently, the research team could also exclude other molecular pathways. For example, they 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, VEGFR3 was ruled out from the indispensable pool of proteins that maintain thyroid vascular integrity.


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Materials provided by Institute for Basic Science. Note: Content may be edited for style and length.


Journal Reference:

  1. Jeon Yeob Jang, Sung Yong Choi, Intae Park, Do Young Park, Kibaek Choe, Pilhan Kim, Young Keum Kim, Byung‐Joo Lee, Masanori Hirashima, Yoshiaki Kubota, Jeong‐Won Park, Sheue‐Yann Cheng, Andras Nagy, Young Joo Park, Kari Alitalo, Minho Shong, Gou Young Koh. VEGFR2 but not VEGFR3 governs integrity and remodeling of thyroid angiofollicular unit in normal state and during goitrogenesis. EMBO Molecular Medicine, 2017; e201607341 DOI: 10.15252/emmm.201607341

Cite This Page:

Institute for Basic Science. "A culprit of thyroid's diseases." ScienceDaily. ScienceDaily, 18 May 2017. <www.sciencedaily.com/releases/2017/05/170518085135.htm>.
Institute for Basic Science. (2017, May 18). A culprit of thyroid's diseases. ScienceDaily. Retrieved May 25, 2017 from www.sciencedaily.com/releases/2017/05/170518085135.htm
Institute for Basic Science. "A culprit of thyroid's diseases." ScienceDaily. www.sciencedaily.com/releases/2017/05/170518085135.htm (accessed May 25, 2017).

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