HISTOLOGY AND HISTOPATHOLOGY

From Cell Biology to Tissue Engineering

 

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

Jessica Vanderstraeten1, Hanane Derradji2, Julie Craps1, Pierre Sonveaux3, Ides M. Colin4, Marie-Christine Many1 and Anne-Catherine Gérard1*

1Pole of Experimental Morphology, Institute of Experimental and Clinical Research (IREC), Catholic University of Louvain (UCL), Brussels, 2Radiobiology Unit, Belgian Nuclear Research Centre (SCK-CEN), Mol, 3Pole of Pharmacology and Therapeutics, Institute of Experimental and Clinical Research (IREC), Catholic University of Louvain (UCL), Brussels and 4Department of Endocrinology and Diabetology, Regional Hospital Center (CHR) Mons-Hainaut, Belgium
*Present address: Department of Endocrinology and Diabetology, Regional Hospital Center (CHR) Mons-Hainaut, Belgium and Institute of life sciences (ISV), Catholic University of Louvain (UCL), Belgium

Offprint requests to: Marie-Christine Many, Pole de Morphologie Expérimentale, Avnue Monier 52, box B1-52.04, Bussels, 1200, Belgium. e-mail: marie-christine.many@uclouvain.be


Summary. 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, VEGF-dependent increase in blood flow. In the gastric mucosa, ID transiently increased VEGF expression in the mucin-secreting 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. Histol Histopathol 31, 897-909 (2016)

Key words: Iodine deficiency, Salivary glands, Stomach, Microvasculature, VEGF

DOI: 10.14670/HH-11-727