Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 오구택 | * |
dc.date.accessioned | 2016-08-29T11:08:56Z | - |
dc.date.available | 2016-08-29T11:08:56Z | - |
dc.date.issued | 2009 | * |
dc.identifier.issn | 0958-0670 | * |
dc.identifier.other | OAK-5282 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/231858 | - |
dc.description.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. | * |
dc.language | English | * |
dc.title | Dexamethasone differentially regulates renal and duodenal calcium-processing genes in calbindin-D9k and -D28k knockout mice | * |
dc.type | Article | * |
dc.relation.issue | 1 | * |
dc.relation.volume | 94 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 138 | * |
dc.relation.lastpage | 151 | * |
dc.relation.journaltitle | Experimental Physiology | * |
dc.identifier.doi | 10.1113/expphysiol.2008.044339 | * |
dc.identifier.wosid | WOS:000261961800016 | * |
dc.identifier.scopusid | 2-s2.0-58149127357 | * |
dc.author.google | Kim M.-H. | * |
dc.author.google | Lee G.-S. | * |
dc.author.google | Jung E.-M. | * |
dc.author.google | Choi K.-C. | * |
dc.author.google | Oh G.-T. | * |
dc.author.google | Jeung E.-B. | * |
dc.contributor.scopusid | 오구택(7007056663) | * |
dc.date.modifydate | 20240123094756 | * |