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

dc.contributor.authorVanderstraeten, Jessica
dc.contributor.authorDerradji, Hanane
dc.contributor.authorCraps, Julie
dc.contributor.authorSonveaux, Pierre
dc.contributor.authorColin, Ides M.
dc.contributor.authorMany, Marie Christine
dc.contributor.authorGérard, Anne Catherine
dc.date.accessioned2021-10-22T08:08:02Z
dc.date.available2021-10-22T08:08:02Z
dc.date.issued2016
dc.description.abstractDespite 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.es
dc.formatapplication/pdfes
dc.format.extent13es
dc.identifier.citationHistology and Histopathology, Vol.31, nº8, (2016)
dc.identifier.doiDOI: 10.14670/HH-11-727
dc.identifier.issn0213-3911
dc.identifier.issn1699-5848
dc.identifier.urihttp://hdl.handle.net/10201/113203
dc.languageenges
dc.publisherUniversidad de Murcia. Departamento de Biología Celular e Histologíaes
dc.relationSin financiación externa a la Universidades
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectIodine deficiencyes
dc.subjectSalivary glandses
dc.subjectStomaches
dc.subjectMicrovasculaturees
dc.subjectVEGFes
dc.subject.otherCDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncologíaes
dc.titleIodine deficiency induces a VEGF-dependent microvascular response in salivary glands and in the stomaches
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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