Linked Life Data

17332530

Source:http://linkedlifedata.com/resource/pubmed/id/17332530

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2007-3-2
pubmed:abstractText
Nitric oxide (NO) is a free radical that mediates a wide array of cell functions. It is generated from l-arginine by NO-synthase (NOS). Expression of NOS isoforms has been demonstrated in thyroid cells. Previous reports indicated that NO donors induce dedifferentiation in thyrocytes. However, the functional significance of endogenous thyrocyte-produced NO has not been explored. This work aimed to study the influence of endogenous NO on parameters of thyroid cell function and differentiation in FRTL-5 cells. We observed that treatment with the NOS inhibitor, Nomega-nitro-L-arginine methyl ester (L-NAME), increased the TSH-stimulated iodide uptake. The TSH-induced sodium iodide symporter (NIS) and thyroglobulin (TG) mRNA expressions were increased after incubation with L-NAME. In transient transfection assays, TSH-stimulated transcriptional activities of NIS and TG promoters were increased by L-NAME. An increment of the TSH-stimulated cell proliferation was observed after NOS inhibition. Similar results were obtained when the action of another NOS inhibitor, N(g)-monomethyl-L-arginine, was analysed for most of these studies. The production of NO, which was not detectable in basal conditions, was increased by TSH. Our data provide strong evidence that endogenous NO could act as a negative signal for TSH-stimulated iodide uptake and thyroid-specific gene expression as well as proliferation in thyrocytes. These findings reveal a possible new inhibitory pathway in the regulation of thyroid cell function.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0022-0795
pubmed:author
pubmed:issnType
Print
pubmed:volume
192
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
627-37
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:17332530-Animals, pubmed-meshheading:17332530-Blotting, Northern, pubmed-meshheading:17332530-Carbazoles, pubmed-meshheading:17332530-Cell Line, pubmed-meshheading:17332530-Cell Proliferation, pubmed-meshheading:17332530-Gene Expression, pubmed-meshheading:17332530-Indoles, pubmed-meshheading:17332530-Iodides, pubmed-meshheading:17332530-NG-Nitroarginine Methyl Ester, pubmed-meshheading:17332530-Nitric Oxide, pubmed-meshheading:17332530-Nitric Oxide Synthase, pubmed-meshheading:17332530-Promoter Regions, Genetic, pubmed-meshheading:17332530-RNA, Messenger, pubmed-meshheading:17332530-Rats, pubmed-meshheading:17332530-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:17332530-Symporters, pubmed-meshheading:17332530-Thyroglobulin, pubmed-meshheading:17332530-Thyroid Gland, pubmed-meshheading:17332530-Thyrotropin, pubmed-meshheading:17332530-Transfection
pubmed:year
2007
pubmed:articleTitle
Endogenous thyrocyte-produced nitric oxide inhibits iodide uptake and thyroid-specific gene expression in FRTL-5 thyroid cells.
pubmed:affiliation
Centro de Investigaciones en Bioquímica Clínica e Inmunología, Consejo Nacional de Investigaciones Científicas y Técnicas, Departamento de Bioquímica Clínica, Universidad Nacional de Córdoba, Haya de la Torre y Medina Allende, 5000 Córdoba, Argentina.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't