徳島大学 教育・研究者情報データベース(EDB)

1. (英) Takei Yuichiro

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2. 山本 浩範

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3. (英) Sato Tadatoshi

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4. (英) Otani Ayako

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5. (英) Kozai Mina

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6. (英) Masuda Masashi

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7. 竹谷 豊([徳島大学.大学院医歯薬学研究部.医学域.栄養科学部門.医科栄養学系.臨床食管理学])

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8. (英) Muto-Sato Kazusa

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9. (英) Lanske Beate

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10. 武田 英二

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(英) Stanniocalcin 2 is associated with ectopic calcification in α-klotho mutant mice and inhibits hyperphosphatemia-induced calcification in aortic vascular smooth muscle cells.

(英) Ectopic calcification of soft tissues can have severe clinical consequences especially when localized to vital organs such as heart, arteries and kidneys. Mammalian stanniocalcin (STC) 1 and 2 are glycoprotein hormones identified as calcium/phosphate-regulating hormones. The mRNA of STCs is upregulated in the kidney of α-klotho mutant (kl/kl) mice, which have hypercalcemia, hyperphosphatemia and hypervitaminosis D and exhibit a short life span, osteopenia and ectopic calcification. In the present study, we investigated the distribution and localization of STCs in kl/kl mice. Quantitative RT-PCR revealed that renal mRNA expression of STC2 was increased in both kl/kl mice and fibroblast growth factor 23 (Fgf23)-null mice compared with wild type mice. Interestingly, STC2 protein was focally localized with the calcified lesions of renal arterioles, renal tubular cells, heart and aorta in kl/kl mice. In vitro analysis of rat aortic vascular smooth muscle (A-10) cells showed that inorganic phosphate (Pi) stimulation significantly increased STC2 mRNA levels as well as that of osteocalcin, osteopontin and the type III sodium-dependent phosphate co-transporter (PiT-1), and induced STC2 secretion. Interestingly, the knockdown with a small interfering RNA or the over-expression of STC2 showed acceleration and inhibition of Pi-induced calcification in A-10 cells, respectively. These results suggest that the up-regulation of STC2 gene expression resulting from abnormal α-klotho-Fgf23 signaling may contribute to limitation of ectopic calcification and thus STC2 represents a novel target gene for cardio-renal syndrome.

1. (英) Animals
2. (英) Aorta
3. (英) Calcinosis
4. (英) Fibroblast Growth Factors
5. (英) Gene Expression Profiling
6. (英) Gene Expression Regulation
7. (英) Glycoproteins
8. (英) Humans
9. 高リン血症(hyperphosphatemia)
10. (英) In Situ Hybridization
11. (英) Kidney
12. (英) Mice
13. (英) Mice, Mutant Strains
14. (英) Muscle, Smooth, Vascular
15. 心筋(myocardium)
16. (英) Myocytes, Smooth Muscle
17. (英) Organ Specificity
18. (英) Phosphates
19. (英) Protein Transport
20. (英) RNA, Messenger
21. (英) Rats
22. (英) Receptors, Cell Surface

1. (英) Article.Affiliation: Department of Clinical Nutrition, Institute of Health Biosciences, University of Tokushima Graduate School, Kuramoto-cho 3, Tokushima 770-8503, Japan.

2. (英) Article.PublicationTypeList.PublicationType: Journal Article

3. (英) Article.PublicationTypeList.PublicationType: Research Support, Non-U.S. Gov't