Colocalization of 11beta-hydroxysteroid dehydrogenase type I and glucocorticoid receptor and its significance in rat hippocampus.
- Author:
Shun-Lun WAN
1
;
Mao-Yao LIAO
;
Ru-Song HAO
;
Zhao-Feng LI
;
Gang SUN
Author Information
1. Department of Physiology, The Second Military Medical University, Shanghai 200433.
- Publication Type:Journal Article
- MeSH:
11-beta-Hydroxysteroid Dehydrogenases;
genetics;
metabolism;
Animals;
Animals, Newborn;
Dexamethasone;
pharmacology;
Gene Expression Regulation;
Hippocampus;
cytology;
metabolism;
Mifepristone;
pharmacology;
Neurons;
chemistry;
metabolism;
PC12 Cells;
Promoter Regions, Genetic;
Rats;
Receptors, Glucocorticoid;
genetics;
metabolism;
Transfection
- From:
Acta Physiologica Sinica
2002;54(6):473-478
- CountryChina
- Language:Chinese
-
Abstract:
This paper was designed to observe the colocalization of 11beta-HSD1 and GR, and its significance in the rat hippocampus. Immunocytochemical dual-staining showed that not only 11beta-HSD1 but also GR immunoreactive substances were present in the cultured rat hippocampal neurons. Moreover, they were colocalized in the same hippocampal neuron. Synthetic glucocorticoid dexamethasone (DEX) up-regulated the protein expression and activity of 11beta-HSD1 in the cultured hippocampal neurons, as determined by Western blot and thin layer chromatography (TLC) respectively. The transfection of PC12 cells with the plasmid containing promoter sequence of 11beta-HSD1 gene and the reporter gene of CAT enzyme was conducted. DEX up-regulated the reporter gene expression in the system described above. The up-regulation of 11beta-HSD1 and reporter gene expression induced by DEX were both blocked by GR antagonist RU38486. Our study suggests that the colocalization of 11beta-HSD1 and GR in the hippocampus may be implicated in the up-regulation of 11beta-HSD1 expression by glucocorticoids combining to its promoter region, which in turn produces more biologically active glucocorticoids necessary for the binding of low affinity of GR.
