期刊
STEROIDS
卷 75, 期 8-9, 页码 555-559出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.steroids.2009.12.001
关键词
Vitamin D; Vitamin D receptor; Cardiomyocytes; Cardiac contractility; Caveolin-3
资金
- NHLBI NIH HHS [R01 HL074894, R01 HL074894-03, R01 HL074894-01, R01 HL074894-02, R01 HL074894-04] Funding Source: Medline
The active form of vitamin D, 1 alpha,25-dihydroxyvitamin D-3 (1,25(OH)(2)D-3), mediates both genomic and rapid non-genomic actions in heart cells. We have previously shown that the vitamin D receptor (VDR) is located in the t-tubular structure of cardiomyocytes. Here we show that VDR specifically interacts with Caveolin-3 in the t-tubules and sarcolemma of adult rat cardiac myocytes. Co-immunoprecipitation studies using VDR antibodies revealed that Caveolin-3 specifically co-precipitates with the VDR and similarly the VDR is co-precipitated with Caveolin-3 antibody. Confocal immuno-fluorescence microscopy analysis also showed co-localization of VDR and Caveolin-3 in t-tubules and sarcolemma. The non-genomic effects of the functional VDR were studied in electrically stimulated myocytes isolated from adult rat hearts. Sarcomere shortening and re-lengthening were measured in 1,25(OH)(2)D-3 treated cardiac myocytes. A 1 nM treatment decreased peak shortening within minutes, suggesting a rapid effect through the membrane-bound VDR. This novel finding of the interaction between VDR and Caveolin-3 is fundamentally important in understanding 1,25(OH)2D3 signal transduction in heart cells and provides further evidence that VDR plays a role in regulation of heart structure and function. (C) 2009 Elsevier Inc. All rights reserved.
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