This Article Full Text Full Text (PDF) All Versions of this Article: 52/6/1106    most recent HYPERTENSIONAHA.108.119602v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Chen, S. Articles by Gardner, D. G. Search for Related Content PubMed PubMed Citation Articles by Chen, S. Articles by Gardner, D. G. Pubmed/NCBI databases Gene GEO Profiles HomoloGene Protein UniGene Compound via MeSH Substance via MeSH Related Collections Cardio-renal physiology/pathophysiology Gene expression Gene regulation Hypertrophy Receptor pharmacology

(Hypertension. 2008;52:1106.)
© 2008 American Heart Association, Inc.

Original Articles

Expression of the Vitamin D Receptor Is Increased in the Hypertrophic Heart

Songcang Chen; Denis J. Glenn; Wei Ni; Christopher L. Grigsby; Keith Olsen; Minobu Nishimoto; Christopher S. Law; David G. Gardner

From the Diabetes Center (S.C., D.J.G., W.N., C.L.G., K.O., M.N., C.S.L., D.G.G.) and Department of Medicine (D.J.G. and D.G.G.), University of California at San Francisco.

Correspondence to David G. Gardner, 1109 HSW Diabetes Center, UCSF, 513 Parnassus Ave, San Francisco, CA 94143-0540. E-mail dgardner{at}diabetes.ucsf.edu

The liganded vitamin D receptor (VDR) is thought to play an important role in controlling cardiac function. Specifically, this system has been implicated as playing an antihypertrophic role in the heart. Despite this, studies of VDR in the heart have been limited in number and scope. In the present study, we used a combination of real-time polymerase chain reaction, Western blot analysis, immunofluorescence, and transient transfection analysis to document the presence of functional VDR in both the myocytes and fibroblasts of the heart, as well as in the intact ventricular myocardium. We also demonstrated the presence of 1--hydroxylase and 24-hydroxylase in the heart, 2 enzymes involved in the synthesis and metabolism of 1,25 dihydroxyvitamin D. VDR is shown to interact directly with the human B-type natriuretic peptide gene promoter, a surrogate marker of the transcriptional response to hypertrophy. Of note, induction of myocyte hypertrophy either in vitro or in vivo leads to an increase in VDR mRNA and protein levels. Collectively, these findings suggest that the key components required for a functional 1,25 dihydroxyvitamin D–dependent signaling system are present in the heart and that this putatively antihypertrophic system is amplified in the setting of cardiac hypertrophy.

Key Words: vitamin D • cardiac hypertrophy • nuclear receptors • BNP • cardiac myocyte

This article has been cited by other articles:

				S. Pilz and A. Tomaschitz Vitamin D deficiency and myocardial dysfunction. J. Am. Coll. Cardiol., May 26, 2009; 53(21): 2011 - 2011. [Full Text] [PDF]

				E. Giovannucci Expanding Roles of Vitamin D J. Clin. Endocrinol. Metab., February 1, 2009; 94(2): 418 - 420. [Full Text] [PDF]