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Dexamethasone differentially regulates renal and duodenal calcium-processing genes in calbindin-D9k and -D28k knockout mice

Title
Dexamethasone differentially regulates renal and duodenal calcium-processing genes in calbindin-D9k and -D28k knockout mice
Authors
Kim M.-H.Lee G.-S.Jung E.-M.Choi K.-C.Oh G.-T.Jeung E.-B.
Ewha Authors
오구택
SCOPUS Author ID
오구택scopus
Issue Date
2009
Journal Title
Experimental Physiology
ISSN
0958-0670JCR Link
Citation
vol. 94, no. 1, pp. 138 - 151
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Glucocorticoids (GCs) appear to downregulate active calcium-transporting genes in the duodenum, resulting in GC-induced calcium-absorbing disorder. In this study, we examined the effects of GCs on calcium-processing genes in the duodenum and kidney and the compensatory mechanism in calbindin-D9k (CaBP-9k) and calbindin-D28k (CaBP-28k) knockout (KO) mice. In the duodenum, we observed compensatory increases in transient receptor potential vanilloid 6 (TRPV6) mRNAs in both calbindin KO mice and CaBP-9k transcripts in CaBP-28k KO mice, and their expressions were decreased by addition of a synthetic GC, dexamethasone (Dex, 10 mg kg -1). In addition, the expression of plasma membrane calcium ATPase 1b (PMCA1b) underwent a compensatory increase in CaBP-9k KO mice, and was blocked by Dex, while the mRNA level of duodenal sodium-calcium exchanger 1 was not altered by KO status or Dex. The renal transcriptional levels of TRPV5 in CaBP-9k KO and CaBP-9k in CaBP-28k KO mice were upregulated in a compensatory manner, while the TRPV6 gene was downregulated following treatment with Dex in the kidney of CaBP-28k KO mice. The immunological location of these duodenal proteins as a primary target of Dex-involved regulation was not altered by Dex or KO status. To elucidate potential mechanism(s) of Dex-induced compensatory gene expression, the levels of GC receptor (GR), vitamin D receptor (VDR) and parathyroid hormone receptor (PTHR) mRNA was also measured in these tissues. Duodenal VDR transcripts were induced in a compensatory manner in both types of KO mice, and were decreased by Dex. In addition, serum corticosterone levels in both KO mice were lower than in wild-type mice. In conclusion, these results suggest that duodenal TRPV6 and CaBP-9k genes appear to be a primary target for GC-induced calcium-absorbing disorder, through direct regulation of duodenal VDR transcription. © 2008 The Authors.
DOI
10.1113/expphysiol.2008.044339
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자연과학대학 > 생명과학전공 > Journal papers
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