Publication:
Iodine deficiency induces a VEGF-dependent microvascular response in salivary glands and in the stomach

Thumbnail Image
Files
Vanderstraeten-31-897-909-2016.pdf(18.27 MB)
Date
2016
relationships.isAuthorOfPublication
relationships.isSecondaryAuthorOf
relationships.isDirectorOf
Authors
Vanderstraeten, Jessica ; Derradji, Hanane ; Craps, Julie ; Sonveaux, Pierre ; Colin, Ides M. ; Many, Marie Christine ; Gérard, Anne Catherine
item.page.secondaryauthor
item.page.director
Publisher
Universidad de Murcia. Departamento de Biología Celular e Histología
publication.page.editor
publication.page.department
DOI
DOI: 10.14670/HH-11-727
item.page.type
info:eu-repo/semantics/article
Description
Abstract
Despite efforts to optimize iodine supply in iodine deficient countries, iodine deficiency (ID) remains a global problem worldwide. Activation of the local microvasculature by ID in the thyroid gland aims at improving the local supply of iodide. For this purpose, the thyrocytes secrete vascular endothelial growth factor (VEGF) that acts on adjacent capillaries, via a reactive oxygen species (ROS)/Hypoxia Inducible factor (HIF)- dependent pathway. Beside the thyroid, other organs including salivary glands and the stomach do express the sodium/iodide symporter (NIS) and are able to take iodide up, potentially rendering them sensitive to ID. To verify this hypothesis, ID-induced effects on the local microvasculature were studied in salivary glands and in the stomach. ID was induced by feeding young mice with an iodide-deficient diet and NIS inhibitor perchlorate in the drinking water. In salivary glands, ID induced a transient increase in HIF-1α protein expression accompanied by a transient, VEGFdependent increase in blood flow. In the gastric mucosa, ID transiently increased VEGF expression in the mucinsecreting epithelium and in ghrelin-secreting endocrine cells. These observations suggest that microvascular changes in response to ID occur in NIS-expressing tissues other than the thyroid. NIS expressing cells could be viewed as iodide sensors that respond to ID by inducing vascular changes, probably to optimize iodide bioavailability at regional or systemic levels.
publication.page.subject
Iodine deficiency , Salivary glands , Stomach , Microvasculature , VEGF
Citation
Histology and Histopathology, Vol.31, nº8, (2016)
URI
http://hdl.handle.net/10201/113203
item.page.embargo
Collections
Histology and histopathology Vol.31, nº8 (2016)
Ir a Estadísticas