| First Author | Healy KD | Year | 2005 |
| Journal | Proc Natl Acad Sci U S A | Volume | 102 |
| Issue | 13 | Pages | 4724-8 |
| PubMed ID | 15769857 | Mgi Jnum | J:97370 |
| Mgi Id | MGI:3575342 | Doi | 10.1073/pnas.0501312102 |
| Citation | Healy KD, et al. (2005) Parathyroid hormone decreases renal vitamin D receptor expression in vivo. Proc Natl Acad Sci U S A 102(13):4724-8 |
| abstractText | The vitamin D receptor (VDR) is a nuclear transcription factor responsible for mediating the biological activities of 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)]. Renal and parathyroid gland VDR content is an important factor in calcium homeostasis, vitamin D metabolism, and the treatment of secondary hyperparathyroidism and renal osteodystrophy. In these tissues, VDR expression is highly regulated by the calcium and vitamin D status. Although 1,25(OH)(2)D(3) up-regulates VDR expression, hypocalcemia and vitamin D deficiency result in drastically reduced expression of the receptor. The generation of 25-hydroxyvitamin D(3)-1alpha-hydroxylase-null mice, which are incapable of endogenously producing 1,25(OH)(2)D(3), has allowed us to investigate the influence of parathyroid hormone (PTH) on VDR expression independent of PTH-mediated increases in 1,25(OH)(2)D(3). Administration of human PTH (1-34) (110 mug/kg per day) for 48 h reduced renal VDR levels from 515 to 435 fmol/mg protein (15%, P < 0.03) in wild-type mice. In the 25-hydroxyvitamin D(3)-1alpha-hydroxylase-null mice, PTH administration strongly reduced renal VDR levels, from 555 to 394 fmol/mg protein (29%, P < 0.001). These results demonstrate that PTH is a potent down-regulator of VDR expression in vivo. |
