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J Biol Chem, Vol. 273, Issue 23, 14575-14581, June 5, 1998

Regulation of Type II Renal Na⁺-dependent Inorganic Phosphate Transporters by 1,25-Dihydroxyvitamin D₃
IDENTIFICATION OF A VITAMIN D-RESPONSIVE ELEMENT IN THE HUMAN NAPI-3 GENE

Yutaka Taketani, Hiroko Segawa, Mika Chikamori, Kyoko Morita, Keiko Tanaka, Shinsuke Kido, Hironori Yamamoto, Yuka Iemori, Sawako Tatsumi, Naoko Tsugawa, Toshio Okano, Tadashi Kobayashi, Ken-ichi Miyamoto, and Eiji Takeda

From the Department of Clinical Nutrition, School of Medicine, University of Tokushima, Tokushima 770-8503, Japan and the  Department of Hygienic Sciences, Kobe Pharmaceutical University, Kobe 658, Japan

Vitamin D is an important regulator of phosphate homeostasis. The effects of vitamin D on the expression of renal Na⁺-dependent inorganic phosphate (P_i) transporters (types I and II) were investigated. In vitamin D-deficient rats, the amounts of type II Na⁺-dependent P_i transporter (NaPi-2) protein and mRNA were decreased in the juxtamedullary kidney cortex, but not in the superficial cortex, compared with control rats. The administration of 1,25-dihydroxyvitamin D₃ (1,25-(OH)₂D₃) to vitamin D-deficient rats increased the initial rate of P_i uptake as well as the amounts of NaPi-2 mRNA and protein in the juxtamedullary cortex. The transcriptional activity of a luciferase reporter plasmid containing the promoter region of the human type II Na⁺-dependent P_i transporter NaPi-3 gene was increased markedly by 1,25-(OH)₂D₃ in COS-7 cells expressing the human vitamin D receptor. A deletion and mutation analysis of the NaPi-3 gene promoter identified the vitamin D-responsive element as the sequence 5'-GGGGCAGCAAGGGCA-3' nucleotides 1977 to 1963 relative to the transcription start site. This element bound a heterodimer of the vitamin D receptor and retinoid X receptor, and it enhanced the basal transcriptional activity of the promoter of the herpes simplex virus thymidine kinase gene in an orientation-independent manner. Thus, one mechanism by which vitamin D regulates P_i homeostasis is through the modulation of the expression of type II Na⁺-dependent P_i transporter genes in the juxtamedullary kidney cortex.

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