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  • Title: Glucocorticoid receptor plays an indispensable role in mineralocorticoid receptor-dependent transcription in GR-deficient BE(2)C and T84 cells in vitro.
    Author: Tsugita M, Iwasaki Y, Nishiyama M, Taguchi T, Shinahara M, Taniguchi Y, Kambayashi M, Nishiyama A, Gomez-Sanchez CE, Terada Y, Hashimoto K.
    Journal: Mol Cell Endocrinol; 2009 Apr 10; 302(1):18-25. PubMed ID: 19146914.
    Abstract:
    The mineralocorticoid receptor (MR) plays an important functional role in the central nervous system; however, the molecular mechanism of MR-dependent gene expression is not entirely clear. In this study, we examined the MR-dependent transcriptional regulation using a human neuronal cell line BE(2)C and an MR/GR-dependent reporter gene (HRE-luciferase) in vitro. Western blot analysis revealed that the cell line expresses MR but not glucocorticoid receptor (GR). In this experimental condition, unexpectedly, the MR-specific ligand aldosterone did not induce HRE-dependent transcription in a native or MR-overexpressed condition, whereas significant transcriptional induction by aldosterone was observed when the GR was co-expressed. The effect of aldosterone was completely inhibited by the MR antagonist spironolactone, indicating an MR-dependent effect. We found similar results in T84 colonic cells expressing neither MR nor GR, such that the aldosterone effect was obtained only when both receptors were co-expressed. The co-operative effect of GR was not obvious with the dimer-deficient mutant GR. Finally, the above findings were reproducible with different promoters containing HRE such as ENaC and MMTV. These results suggest that GR plays an indispensable role in MR-dependent transcription, possibly by forming a MR/GR heterodimer or by acting as a co-activator of MR/MR homodimer.
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