Vitamin D receptor is required for dietary calcium-induced repression of calbindin-D9k expression in mice.

Calbindin (CaBP), the vitamin D-dependent calcium-binding protein, is believed to play an important role in intracellular calcium transport. The aim of this study was to investigate the effect of high dietary calcium on the expression of CaBP-D9k and CaBP-D28k in the presence and absence of a functional vitamin D receptor (VDR). Treatment with the HCa-Lac diet containing 2% calcium, 1.

Critical role of vitamin D in sulfate homeostasis: regulation of the sodium-sulfate cotransporter by 1,25-dihydroxyvitamin D3.

As the fourth most abundant anion in the body, sulfate plays an essential role in numerous physiological processes. One key protein involved in transcellular transport of sulfate is the sodium-sulfate cotransporter NaSi-1, and previous studies suggest that vitamin D modulates sulfate homeostasis by regulating NaSi-1 expression. In the present study, we found that, in mice lacking the vitamin D receptor (VDR), NaSi-1 expression in the kidney was reduced by 72% but intestinal NaSi-1 levels remained unchanged.

Regulation of calbindin-D9k expression by 1,25-dihydroxyvitamin D(3) and parathyroid hormone in mouse primary renal tubular cells.

Calbindin (CaBP)-D9k is a major vitamin D target gene involved in calcium homeostasis. However, studies on the molecular mechanisms of CaBP-D9k gene regulation have been hampered by the lack of an appropriate cell culture system. In the present study, we used mouse primary renal tubular cell (PRTC) cultures to investigate the regulation of CaBP-D9k expression by 1,25(OH)(2)D(3).