rdf:type |
|
lifeskim:mentions |
umls-concept:C0001629,
umls-concept:C0007634,
umls-concept:C0025148,
umls-concept:C0040649,
umls-concept:C0042866,
umls-concept:C0205102,
umls-concept:C0206473,
umls-concept:C0332307,
umls-concept:C0687028,
umls-concept:C1335671,
umls-concept:C1515877,
umls-concept:C1516698,
umls-concept:C1550278,
umls-concept:C1879547,
umls-concept:C2709270
|
pubmed:issue |
3
|
pubmed:dateCreated |
2007-7-26
|
pubmed:abstractText |
Many clinical and animal studies suggest that vitamin D and its metabolites have beneficial effects in the cardiovascular and renal systems. Using immunologic and enzymatic assays, vitamin D receptor and 25 hydroxyvitamin D3 1alpha-hydroxylase activity were found in inner medullary collecting duct (IMCD) cells suggesting an autocrine/paracrine role in this nephron segment. In this study, we examined the ability of 1,25 dihydroxyvitamin D3 (1,25(OH)(2)D3) to regulate the expression of the vasculoprotective natriuretic peptide receptor-A gene in these cells in culture. Treatment of the cells with 1,25(OH)(2)D3 caused a doubling of natriuretic peptide-dependent cyclic guanosine monophosphate production and a significant increase in natriuretic peptide receptor-A protein expression. This was accompanied by significant increases in receptor mRNA levels and gene-promoter activity. Mutation of a vitamin D response element, positioned upstream from the gene start site, resulted in a complete loss of 1,25(OH)(2)D3-dependent induction but not the induction by hypertonic stimuli. Introduction of small interfering RNA directed against the vitamin D receptor into the IMCD cells resulted in decreased natriuretic peptide receptor-A gene promoter activity and protein. The increase in this receptor expression may account for some of the reported beneficial effect of 1,25(OH)(2)D3 on the cardiovascular system and kidney.
|
pubmed:grant |
|
pubmed:commentsCorrections |
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Atrial Natriuretic Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Calcitriol,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channel Agonists,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic GMP,
http://linkedlifedata.com/resource/pubmed/chemical/Guanylate Cyclase,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Small Interfering,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Atrial Natriuretic Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium,
http://linkedlifedata.com/resource/pubmed/chemical/Vitamin D,
http://linkedlifedata.com/resource/pubmed/chemical/atrial natriuretic factor receptor A
|
pubmed:status |
MEDLINE
|
pubmed:month |
Aug
|
pubmed:issn |
0085-2538
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:volume |
72
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
300-6
|
pubmed:dateRevised |
2008-11-21
|
pubmed:meshHeading |
pubmed-meshheading:17440494-Animals,
pubmed-meshheading:17440494-Atrial Natriuretic Factor,
pubmed-meshheading:17440494-Calcitriol,
pubmed-meshheading:17440494-Calcium Channel Agonists,
pubmed-meshheading:17440494-Cardiovascular Physiological Phenomena,
pubmed-meshheading:17440494-Cells, Cultured,
pubmed-meshheading:17440494-Cyclic GMP,
pubmed-meshheading:17440494-Guanylate Cyclase,
pubmed-meshheading:17440494-Kidney Tubules, Collecting,
pubmed-meshheading:17440494-RNA, Messenger,
pubmed-meshheading:17440494-RNA, Small Interfering,
pubmed-meshheading:17440494-Rats,
pubmed-meshheading:17440494-Rats, Sprague-Dawley,
pubmed-meshheading:17440494-Receptors, Atrial Natriuretic Factor,
pubmed-meshheading:17440494-Sodium,
pubmed-meshheading:17440494-Transcription, Genetic,
pubmed-meshheading:17440494-Vitamin D
|
pubmed:year |
2007
|
pubmed:articleTitle |
Vitamin D activates type A natriuretic peptide receptor gene transcription in inner medullary collecting duct cells.
|
pubmed:affiliation |
Diabetes Center, University of California at San Francisco, San Francisco, California 94143-0540, USA. schen@diabetes.ucsf.edu
|
pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
|