Source:http://linkedlifedata.com/resource/pubmed/id/16289840
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
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| pubmed:dateCreated |
2006-1-13
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| pubmed:abstractText |
11beta-Hydroxysteroid dehydrogenase type 2 is a glucocorticoid metabolizing enzyme that catalyzes rapid inactivation of corticosterone and cortisol to inert 11-keto derivatives. As 11beta-hydroxysteroid dehydrogenase type 2 is highly expressed in the developing brain, but not in the adult CNS, we hypothesized that it may represent a protective barrier to the deleterious actions of corticosteroids on proliferating cells. To test this hypothesis we have investigated the development and growth of the cerebellum in neonatal C57BL/6 mice and mice lacking 11beta-hydroxysteroid dehydrogenase type 2 (-/-). 11beta-Hydroxysteroid dehydrogenase type 2-/- mice had consistently lower body weight throughout the neonatal period, coupled with a smaller brain size although this was normalized when corrected for body weight. The cerebellar size was smaller in 11beta-hydroxysteroid dehydrogenase type 2-/- mice, due to decreases in size of both the molecular and internal granule layers. When exogenous corticosterone was administered to the pups between postnatal days 4 and 13, 11beta-hydroxysteroid dehydrogenase type 2(-/-) mice were more sensitive, showing further inhibition of cerebellar growth while the wildtype mice were not affected. Upon withdrawal of exogenous steroid, there was a rebound growth spurt so that at day 21 postnatally, the cerebellar size in 11beta-hydroxysteroid dehydrogenase type 2-/- mice was similar to untreated mice of the same genotype. Furthermore, 11beta-hydroxysteroid dehydrogenase type 2-/- mice had a delay in the attainment of neurodevelopmental landmarks such as negative geotaxis and eye opening. We therefore suggest that 11beta-hydroxysteroid dehydrogenase type 2 acts as to protect the developing nervous system from the deleterious consequences of glucocorticoid overexposure.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Feb
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| pubmed:issn |
0306-4522
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
137
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
865-73
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| pubmed:dateRevised |
2008-11-21
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| pubmed:meshHeading |
pubmed-meshheading:16289840-11-beta-Hydroxysteroid Dehydrogenase Type 2,
pubmed-meshheading:16289840-Animals,
pubmed-meshheading:16289840-Animals, Newborn,
pubmed-meshheading:16289840-Body Weight,
pubmed-meshheading:16289840-Brain,
pubmed-meshheading:16289840-Cell Proliferation,
pubmed-meshheading:16289840-Cerebellum,
pubmed-meshheading:16289840-Corticosterone,
pubmed-meshheading:16289840-Female,
pubmed-meshheading:16289840-Glial Fibrillary Acidic Protein,
pubmed-meshheading:16289840-Glucocorticoids,
pubmed-meshheading:16289840-Immunohistochemistry,
pubmed-meshheading:16289840-In Situ Hybridization,
pubmed-meshheading:16289840-Male,
pubmed-meshheading:16289840-Mice,
pubmed-meshheading:16289840-Mice, Inbred C57BL,
pubmed-meshheading:16289840-Mice, Knockout,
pubmed-meshheading:16289840-Organ Size,
pubmed-meshheading:16289840-Postural Balance,
pubmed-meshheading:16289840-Reflex
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| pubmed:year |
2006
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| pubmed:articleTitle |
11beta-Hydroxysteroid dehydrogenase type 2 protects the neonatal cerebellum from deleterious effects of glucocorticoids.
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| pubmed:affiliation |
Endocrinology Unit, Centre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK. Megan.Holmes@ed.ac.uk
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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