ISSN:
0730-2312
Keywords:
PKC
;
1,25-dihydroxyvitamin D3
;
vitamin D receptor
;
VDR
;
rat
;
Life and Medical Sciences
;
Cell & Developmental Biology
Source:
Wiley InterScience Backfile Collection 1832-2000
Topics:
Biology
,
Chemistry and Pharmacology
,
Medicine
Notes:
Effects of protein kinase C (PKC) inhibitor and activator on 1,25(OH)2D3-induced gene expression were examined in rat intestinal epithelial cells, IEC-6 cells. A potent PKC inhibitor, H-7 (20 μM), completely abated 1,25(OH)2D3-induced 24-hydroxylase gene expression at 3 and 6 h. The effect of H-7 was dose dependent with IC50 around 5 μM. Other protein kinase inhibitors, HA-1004 and H-89 (20 μM), had no effects. Furthermore, the activation of PKC by 12-O-tetradecanoylphorbol-13-acetate (TPA) potentiated the effect of 1,25(OH)2D3 by 1 h. TPA appeared to exert its effect at a transcriptional step, since mRNA stability was not affected by TPA treatment. At 3 h after the treatment of the cells with H-7 and TPA, vitamin D receptor (VDR) contents estimated by 3H-1,25(OH)2D3 binding capacity were 72.4 and 63.2% of vehicle-treated cells without significant changes of binding affinities, suggesting that the effect of H-7 and TPA was not the result of changes in VDR content or its binding affinity. In conclusion, PKC is involved in 1,25(OH)2D3-induced 24-hydroxylase gene expression in IEC-6 cells between 1,25(OH)2D3-VDR binding and VDR-induced gene transactivation. © 1994 Wiley-Liss, Inc.
Additional Material:
7 Ill.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1002/jcb.240550210
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