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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2008-3-6
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pubmed:abstractText |
Intracellular adhesion molecule-1 (ICAM-1) expression on the thyroid follicular cells of non-obese diabetic (NOD).H2(h4) mice is enhanced by iodide treatment, which correlates with autoimmune thyroid disease in genetically susceptible NOD.H2(h4) mice. The current study examines the mechanism of iodine-enhanced up-regulation of ICAM-1 on the surface of thyroid cells. We hypothesized that the up-regulation of ICAM-1 is due to a transient increase in production of reactive oxygen species (ROS). ROS may initiate signalling of the ICAM-1 gene promoter, enhancing up-regulated ICAM-1 protein on the cell surface. Single-cell suspensions of thyroid follicular cells from thyroiditis-susceptible NOD.H2(h4) or non-susceptible BALB/c mice were treated in vitro with sodium iodide. Extracellular and intracellular ROS were assessed by luminol-derived chemiluminescence and flow cytometry assays respectively. Our results demonstrate that thyroid follicular cells of NOD.H2(h4) generate higher levels of ROS compared with cells from non-susceptible strains of mice. Expression of a subunit protein of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, p67(phox), was analysed by Western blot immunoassay. A constitutive expression of the p67(phox) subunit protein was observed in NOD.H2(h4) mice prior to iodine treatment. No such expression was found in BALB/c mice. Treatment of NOD.H2(h4) thyroid cells with diphenyleneiodium, an inhibitor of NADPH oxidase, reduced generation of ROS and of ICAM-1 protein expression. Thus, thyrocytes from NOD.H2(h4) mice produce enhanced levels of ROS that may be mediated by NADPH oxidase. Consequently, in NOD.H2(h4) mice the ROS-induced signal for ICAM-1 up-regulation may contribute to mononuclear cellular infiltration of the thyroid gland and the progression of autoimmune thyroid disease.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-1009939,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-10198242,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-10201926,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-10222025,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-10401672,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-10614768,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-10614785,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-10806195,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-11224519,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-11279538,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-11396699,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-11736644,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-11936473,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-12244202,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-12565790,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-12645626,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-12759429,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-1373059,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-15623762,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-15944276,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-16232211,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-1708262,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-17131377,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-2401227,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-2671237,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-4048936,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-5133731,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-7626551,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-7642556,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-7751500,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-8095960,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-8350054,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-8938107,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-9442038,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18241232-9590262
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
1365-2249
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
152
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
13-20
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:18241232-Animals,
pubmed-meshheading:18241232-Cells, Cultured,
pubmed-meshheading:18241232-Diabetes Mellitus, Type 1,
pubmed-meshheading:18241232-Enzyme Inhibitors,
pubmed-meshheading:18241232-Female,
pubmed-meshheading:18241232-Intercellular Adhesion Molecule-1,
pubmed-meshheading:18241232-Male,
pubmed-meshheading:18241232-Mice,
pubmed-meshheading:18241232-Mice, Inbred BALB C,
pubmed-meshheading:18241232-Mice, Inbred NOD,
pubmed-meshheading:18241232-Nitric Oxide Synthase,
pubmed-meshheading:18241232-Onium Compounds,
pubmed-meshheading:18241232-Phosphoproteins,
pubmed-meshheading:18241232-Reactive Oxygen Species,
pubmed-meshheading:18241232-Sodium Iodide,
pubmed-meshheading:18241232-Thyroid Gland,
pubmed-meshheading:18241232-Thyroiditis, Autoimmune,
pubmed-meshheading:18241232-Up-Regulation
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pubmed:year |
2008
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pubmed:articleTitle |
Intracellular adhesion molecule-1 up-regulation on thyrocytes by iodine of non-obese diabetic.H2(h4) mice is reactive oxygen species-dependent.
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pubmed:affiliation |
Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD 21205, USA.
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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