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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2003-2-14
pubmed:abstractText
Thyroid hormones are essential for a variety of developmental and metabolic processes. Congenital hypothyroidism (CHT) results in severe defects in the development of different tissues, in particular brain. As an animal model for CHT, we studied Pax8(-/-) mice, which are born without a thyroid gland. We determined the expression of iodothyronine deiodinase D1 in liver and kidney, D2 in brain and pituitary, and D3 in brain, as well as serum T(4), T(3), and rT(3) levels in Pax8(-/-) vs. control mice during the first 3 wk of life. In control mice, serum T(4) and T(3) were undetectable on the day of birth (d 0) and increased to maximum levels on d 15. In Pax8(-/-) mice, serum T(4) and T(3) remained below detection limits. Serum rT(3) was high on d 0 in both groups and rapidly decreased in Pax8(-/-), but not in control mice. Hepatic and renal D1 activities and mRNA levels were low on d 0 and increased in control mice roughly parallel to serum T(4) and T(3) levels. In Pax8(-/-) mice, tissue D1 activities and mRNA levels remained low. Cerebral D2 activities were low on d 0 and increased to maximum levels on d 15, which were approximately 10-fold higher in Pax8(-/-) than in control mice. D2 mRNA levels were higher in Pax8(-/-) than in control mice only on d 21. Cerebral D3 activities and mRNA levels were high on d 0 and showed a moderate decrease between d 3 and 15, with values slightly lower in Pax8(-/-) than in control mice. One day after the injection of 200 ng T(4) or 20 ng T(3)/g body weight, tissue deiodinase activities and mRNA levels were at least partially restored toward control levels, with the exception of cerebral D3 activity. In conclusion, these findings show dramatic age and thyroid state-dependent changes in the expression of deiodinases in central and peripheral tissues of mice during the first 3 wk of life.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
144
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
777-84
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:12586753-Aging, pubmed-meshheading:12586753-Animals, pubmed-meshheading:12586753-Brain, pubmed-meshheading:12586753-Congenital Hypothyroidism, pubmed-meshheading:12586753-DNA-Binding Proteins, pubmed-meshheading:12586753-Disease Models, Animal, pubmed-meshheading:12586753-Female, pubmed-meshheading:12586753-Gene Expression Regulation, Enzymologic, pubmed-meshheading:12586753-Growth Disorders, pubmed-meshheading:12586753-Hypothyroidism, pubmed-meshheading:12586753-Iodide Peroxidase, pubmed-meshheading:12586753-Kidney, pubmed-meshheading:12586753-Liver, pubmed-meshheading:12586753-Male, pubmed-meshheading:12586753-Mice, pubmed-meshheading:12586753-Mice, Knockout, pubmed-meshheading:12586753-Nuclear Proteins, pubmed-meshheading:12586753-Paired Box Transcription Factors, pubmed-meshheading:12586753-Pituitary Gland, pubmed-meshheading:12586753-RNA, Messenger, pubmed-meshheading:12586753-Thyroxine, pubmed-meshheading:12586753-Trans-Activators, pubmed-meshheading:12586753-Triiodothyronine, pubmed-meshheading:12586753-Triiodothyronine, Reverse
pubmed:year
2003
pubmed:articleTitle
Regulation of iodothyronine deiodinases in the Pax8-/- mouse model of congenital hypothyroidism.
pubmed:affiliation
Max Planck Institut für Experimentelle Endokrinologie, D-30625 Hannover, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't