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This Article Accepted manuscript (PDF) All Versions of this Article: JME-08-0161v1 42/3/261    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Takei, Y. Articles by Takeda, E. Search for Related Content PubMed PubMed Citation Articles by Takei, Y. Articles by Takeda, E.

Y Takei, Department of Clinical Nutrition, University of Tokushima Graduate School, Tokushima, Japan
H Yamamoto, Department of Clinical Nutrition, University of Tokushima Graduate School, Tokushima, 770-8503, Japan
M Masuda, Department of Clinical Nutrition, University of Tokushima Graduate School, Tokushima, Japan
T Sato, Department of Clinical Nutrition, University of Tokushima Graduate School, Tokushima, Japan
Y Taketani, Department of Clinical Nutrition, University of Tokushima Graduate School, Tokushima, Japan
E Takeda, Department of Clinical Nutrition, University of Tokushima Graduate School, Tokushima, Japan

Correspondence: Hironori Yamamoto, Email: yamamoto{at}nutr.med.tokushima-u.ac.jp

Abstract

We have previously identified a second mammalian stanniocalcin (STC2) in humans and demonstrated that STC2 inhibits phosphate uptake in an opossum renal proximal tubular cell line (OK cells). However, the regulation of STC2 gene expression in OK cells is not well understood. In this study, we identified the opossum STC2 cDNA sequence. The opossum STC2 amino acid sequence had 78.8% homology with human STC2, and has a conserved putative N-linked glycosylation site. Next, we investigated the regulation of STC2 gene expression by the classical calcium and phosphate-regulating factors 1,25(OH)2D3 and parathyroid hormone (PTH) in OK cells. In western blot analysis using affinity-purified anti-STC2 antibody, the secretion of STC2 protein was stimulated by 1,25(OH)2D3 in a dose-dependent manner. In contrast, PTH suppressed the induction of STC2 protein secretion by 1,25(OH)2D3. Real-time PCR analysis revealed that STC2 mRNA expression was increased by 1,25(OH)2D3 in a dose-dependent and time-dependent manner. In addition, actinomycin D, an RNA synthesis inhibitor, prevented the effects of 1,25(OH)2D3 on STC2 gene expression. On the other hand, PTH and phorbol 12,13-myristic acetate, a specific PKC activator, but not 8-bromo-cyclic AMP, a specific PKA activator, reduced the mRNA levels of STC2. And, Go6976, a specific PKC inhibitor, abolished the down-regulation of STC2 mRNA expression by PTH. Furthermore, we demonstrated that renal STC2 mRNA expression was increased by 1,25(OH)2D3 and decreased by PTH in vivo. These results suggest that STC2 is positively and negatively controlled by 1,25(OH)2D3 and PTH in renal proximal tubular cells.