研究者詳細 - 辰巳佐和子

論文 - 辰巳佐和子

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Vitamin D and type II sodium-dependent phosphate cotransporters. 招待国際誌

Kido S, Kaneko I, Tatsumi S, Segawa H, Miyamoto K.

Contrib Nephrol. 180 86 - 97 2013年5月

Histological examination on osteoblastic activities in the alveolar bone of transgenic mice with induced ablation of osteocytes. 国際誌

Li M, Hasegawa T, Hogo H, Tatsumi S, Liu Z, Guo Y, Sasaki M, Tabata C, Yamamoto T, Ikeda K, Amizuka N.

Histol Histopathol. 28 ( 3 ) 327 - 335 2013年3月

Histological examination on osteoblastic activities in the alveolar bone of transgenic mice with induced ablation of osteocytes 査読

Minqi Li, Tomoka Hasegawa, Hiromi Hogo, Sawako Tatsumi, Zhusheng Liu, Ying Guo, Muneteru Sasaki, Chihiro Tabata, Tsuneyuki Yamamoto, Kyoji Ikeda, Norio Amizuka

HISTOLOGY AND HISTOPATHOLOGY 28 ( 3 ) 327 - 335 2013年3月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：F HERNANDEZ

The purpose of this study was to examine histological alterations on osteoblasts from the alveolar bone of transgenic mice with targeted ablation of osteoctyes. Eighteen weeks-old transgenic mice based on the diphtheria toxin (DT) receptor-mediated cell knockout (TRECK) system were used in these experiments. Mice were injected intraperitoneally with 50 mu g/kg of DT in PBS, or only PBS as control. Two weeks after injections, mice were subjected to transcardiac perfusion with 4% paraformaldehyde in 0.1M phosphate buffer (pH 7.4), and the available alveolar bone was removed for histochemical analyses. Approximately 75% of osteocytes from alveolar bones became apoptotic after DT administration, and most osteocytic lacunae became empty. Osteoblastic numbers and alkaline phosphatase (ALP) activity were markedly reduced at the endosteum of alveolar bone after DT administration compared with the control. Osteoblastic ALP activity in the periodontal ligament region, on the other hand, hardly showed any differences between the two groups even though numbers were reduced in the experiment group. Silver impregnation showed a difference in the distribution of bone canaliculi between the portions near the endosteum and the periodontal ligament: the former appeared regularly arranged in contrast to the latter's irregular distribution. Under transmission electron microscopy (TEM), the osteoblasts in the periodontal ligament showed direct contact with the Sharpey's fibers. Thus, osteoblastic activity was affected by osteocyte ablation in general, but osteoblasts in contact with the periodontal ligament were less affected than endosteal osteoblasts.

DOI： 10.14670/HH-28.327

Web of Science

PubMed

Vitamin D and Type II Sodium-Dependent Phosphate Cotransporters 査読

Shinsuke Kido, Ichiro Kaneko, Sawako Tatsumi, Hiroko Segawa, Ken-ichi Miyamoto

PHOSPHATE AND VITAMIN D IN CHRONIC KIDNEY DISEASE 180 86 - 97 2013年

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：KARGER

The type II sodium-dependent Pi (NaPi) cotransporters (NaPi-IIa, NaPi-IIb and NaPi-IIc) contribute to renal and intestinal Pi absorption. 1,25-Dihydroxyvitamin D [1,25(OH)(2)D-3] is an important factor for NaPi-II transporters in the small intestine and kidney. In a previous study, low levels of 1,25(OH)(2)D-3 appeared to suppress the expression of renal NaPi cotransporters. We identified a functional vitamin D receptor-responsive element in the human NaPi-IIa and NaPi-lIc genes in renal epithelial cells. In an analysis of vitamin D receptor (VDR)-null mice, we observed early onset of hypophosphatemia. The cause of the hypophosphatemia in VDR-null mice before weaning appeared to be increased plasma parathyroid hormone (PTH) levels during the suckling periods. A rescue diet (high calcium diet) decreased plasma PTH levels in VDR-null mice. The reduced plasma PTH levels normalized the renal Npt2a and Npt2c protein levels in weanling animals. Thus, the dietary intervention completely normalized the expression of the renal Pi transporters (Npt2a/Npt2c) in VDR-null mice, suggesting that the lack of VDR activity was not the cause of the impaired renal Pi reabsorption. In suckling animals, 1,25(OH)(2)D-3 may be essential for the prevention of the phosphaturic action of PTH. In adult animals, 1,25(OH)(2)D-3 is thought to be an important factor for posttranscriptional regulation of the Npt2b gene in the small intestine. Fibroblast growth factor 23 (FGF23) is a novel phosphaturic factor that influences vitamin D metabolism and renal reabsorption of Pi. We characterized the role of the VDR in the action of FGF23 using VDR-null mice. FGF23 reduced renal Pi transport and 25-hydroxyvitamin D 1a-hydroxylase levels by a mechanism that was independent of the VDR. By contrast, the induction of 25-hydroxyvitamin D 24-hydroxylase and the reduction in serum 1,25(OH)(2)D-3 levels induced by FGF23 were dependent on the VDR. Thus, the VDR is not essential for the phosphaturic action of FGF23, but is essential for control of the plasma 1,25(OH)(2)D-3 level. Moreover, FGF23 reduces intestinal NaPi transport activity and Npt2b protein levels by a mechanism that is dependent on the VDR. Klotho functions as a co-receptor for FGF23 and is increased by 1,25(OH)(2)D-3. Klotho induces phosphaturia by inhibiting the renal NaPi-Ila transporter. In this review, we discuss the roles of 1,25(OH)(2)D-3/VDR in the regulation of renal type II NaPi cotransporters in the kidney and small intestine. Copyright (C) 2013 S. Karger AG, Basel

DOI： 10.1159/000346786

Web of Science

PubMed

[Information about phosphorus additives and nutritional counseling]. 査読

Kido S, Nomura K, Sasaki S, Shiozaki Y, Segawa H, Tatsumi S

Clinical calcium 22 ( 10 ) 1583 - 1591 2012年10月

[The roles of intestinal and renal sodium dependent phosphate transporters in phosphate homeostasis]. 査読

Segawa H, Sasaki S, Mukai T, Manabe M, Kido S, Tatsumi S, Miyamoto K

Clinical calcium 22 ( 10 ) 1469 - 1476 2012年10月

[Phosphate sensing and intestine]. 査読

Tatsumi S, Nomura K, Miyagawa A, Kido S, Segawa H

Clinical calcium 22 ( 10 ) 1537 - 1541 2012年10月

Processing and stability of type IIc sodium-dependent phosphate cotransporter mutations in patients with hereditary hypophosphatemic rickets with hypercalciuria. 国際誌

Haito-Sugino S, Ito M, Ohi A, Shiozaki Y, Kangawa N, Nishiyama T, Aranami F, Sasaki S, Mori A, Kido S, Tatsumi S, Segawa H, Miyamoto K.

Am J Physiol Cell Physiol. 302 ( 9 ) C1316 - C1330 2012年5月

Processing and stability of type IIc sodium-dependent phosphate cotransporter mutations in patients with hereditary hypophosphatemic rickets with hypercalciuria 査読

Sakiko Haito-Sugino, Mikiko Ito, Akiko Ohi, Yuji Shiozaki, Natsumi Kangawa, Takashi Nishiyama, Fumito Aranami, Shohei Sasaki, Ayaka Mori, Shinsuke Kido, Sawako Tatsumi, Hiroko Segawa, Ken-ichi Miyamoto

AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY 302 ( 9 ) C1316 - C1330 2012年5月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：AMER PHYSIOLOGICAL SOC

Haito-Sugino S, Ito M, Ohi A, Shiozaki Y, Kangawa N, Nishiyama T, Aranami F, Sasaki S, Mori A, Kido S, Tatsumi S, Segawa H, Miyamoto K. Processing and stability of type IIc sodium-dependent phosphate cotransporter mutations in patients with hereditary hypophosphatemic rickets with hypercalciuria. Am J Physiol Cell Physiol 302: C1316-C1330, 2012. First published December 7, 2012; doi:10.1152/ajpcell.00314.2011.-Mutations in the apically located Na+-dependent phosphate (NaPi) cotransporter, SLC34A3 (NaPi-IIc), are a cause of hereditary hypophosphatemic rickets with hypercalciuria (HHRH). We have characterized the impact of several HHRH mutations on the processing and stability of human NaPi-IIc. Mutations S138F, G196R, R468W, R564C, and c. 228delC in human NaPi-IIc significantly decreased the levels of NaPi cotransport activities in Xenopus oocytes. In S138F and R564C mutant proteins, this reduction is a result of a decrease in the V-max for P-i, but not the K-m. G196R, R468W, and c. 228delC mutants were not localized to oocyte membranes. In opossum kidney (OK) cells, cell surface labeling, microscopic confocal imaging, and pulse-chase experiments showed that G196R and R468W mutations resulted in an absence of cell surface expression owing to endoplasmic reticulum (ER) retention. G196R and R468W mutants could be partially stabilized by low temperature. In blue native-polyacrylamide gel electrophoresis analysis, G196R and R468W mutants were either denatured or present in an aggregation complex. In contrast, S138F and R564C mutants were trafficked to the cell surface, but more rapidly degraded than WT protein. The c. 228delC mutant did not affect endogenous NaPi uptake in OK cells. Thus, G196R and R468W mutations cause ER retention, while S138F and R564C mutations stimulate degradation of human NaPi-IIc in renal epithelial cells. Together, these data suggest that the NaPi-IIc mutants in HHRH show defective processing and stability.

DOI： 10.1152/ajpcell.00314.2011

Web of Science

PubMed

Identification and functional analysis of a splice variant of mouse sodium-dependent phosphate transporter Npt2c. 国際誌

Kuwahara S, Aranami F, Segawa H, Onitsuka A, Honda N, Tominaga R, Hanabusa E, Kaneko I, Yamanaka S, Sasaki S, Ohi A, Nomura K, Tatsumi S, Kido S, Ito M, Miyamoto K.

J Med Invest. 59 ( 1,2 ) 116 - 126 2012年2月

Identification and functional analysis of a splice variant of mouse sodium-dependent phosphate transporter Npt2c 査読

Shoji Kuwahara, Fumito Aranami, Hiroko Segawa, Akemi Onitsuka, Naoko Honda, Rieko Tominaga, Etsuyo Hanabusa, Ichiro Kaneko, Setsuko Yamanaka, Shohei Sasaki, Akiko Ohi, Kengo Nomura, Sawako Tatsumi, Shinsuke Kido, Mikiko Ito, Ken-Ichi Miyamoto

Journal of Medical Investigation 59 ( 1-2 ) 116 - 126 2012年2月

記述言語：英語掲載種別：研究論文（学術雑誌）

Mutations in the SLC34A3 gene, a sodium-dependent inorganic phosphate (Pi) cotransporter, also referred to as NaPi IIc, causes hereditary hypophosphatemic rickets with hypercalciuria (HHRH), an autosomal recessive disorder. In human and rodent, NaPi IIc is mainly localized in the apical membrane of renal proximal tubular cells. In this study, we identified mouse NaPi IIc variant (Npt2c-v1) that lacks the part of the exon 3 sequence that includes the assumed translation initiation site of Npt2c. Microinjection of mouse Npt2c-v1 cRNA into Xenopus oocytes demonstrated that Npt2c-v1 showed sodium-dependent Pi cotransport activity. The characterization of pH dependency showed activation at extracellular alkaline-pH. Furthermore, Npt2c-v1 mediated Pi transport activity was significantly higher at any pH value than those of Npt2c. In an in vitro study, the localization of the Npt2c-v1 protein was detected in the apical membrane in opossum kidney cells. The expression of Npt2c-v1 mRNA was detected in the heart, spleen, testis, uterus, placenta, femur, cerebellum, hippocampus, diencephalon and brain stem of mouse. Using mouse bone primary cultured cells, we showed the expression of Npt2c-v1 mRNA. In addition, the Npt2c protein was detected in the spermatozoa head. Thus, Npt2c-v1 was expressed in extra-renal tissues such as epididymal spermatozoa and may function as a sodium-dependent phosphate transporter.

DOI： 10.2152/jmi.59.116

Scopus

PubMed

[Fibroblast growth factor 23 mediates the phosphaturic actions of cadmium]. 査読

Kido S, Fujihara M, Nomura K, Sasaki S, Shiozaki Y, Segawa H, Tatsumi S, Miyamoto K

Nihon eiseigaku zasshi. Japanese journal of hygiene 67 ( 4 ) 464 - 471 2012年

Inorganic phosphate homeostasis in sodium-dependent phosphate cotransporter Npt2b⁺/⁻ mice. 国際誌

Ohi A, Hanabusa E, Ueda O, Segawa H, Horiba N, Kaneko I, Kuwahara S, Mukai T, Sasaki S, Tominaga R, Furutani J, Aranami F, Ohtomo S, Oikawa Y, Kawase Y, Wada NA, Tachibe T, Kakefuda M, Tateishi H, Matsumoto K, Tatsumi S, Kido S, Fukushima N, Jishage K, Miyamoto K.

Am J Physiol Renal Physiol. 301 ( 5 ) F1105 - F1113 2011年11月

Inorganic phosphate homeostasis in sodium-dependent phosphate cotransporter npt2b +/-mice 査読

Akiko Ohi, Etsuyo Hanabusa, Otoya Ueda, Hiroko Segawa, Naoshi Horiba, Ichiro Kaneko, Shoji Kuwahara, Tomo Mukai, Shohei Sasaki, Rieko Tominaga, Junya Furutani, Fumito Aranami, Shuichi Ohtomo, Yumiko Oikawa, Yousuke Kawase, Naoko A. Wada, Takanori Tachibe, Mami Kakefuda, Hiromi Tateishi, Kaoru Matsumoto, Sawako Tatsumi, Shinsuke Kido, Naoshi Fukushima, Kou-ichi Jishage, Ken-ichi Miyamoto

American Journal of Physiology - Renal Physiology 301 ( 5 ) F1105 - F1113 2011年11月

記述言語：英語掲載種別：研究論文（学術雑誌）

An inorganic phosphate (P i)-restricted diet is important for patients with chronic kidney disease and patients on hemodialysis. Phosphate binders are essential for preventing hyperphosphatemia and ectopic calcification. The sodium-dependent P i (Na/P i) transport system is involved in intestinal Pi absorption and is regulated by several factors. The type II sodium-dependent P i transporter Npt2b is expressed in the brush-border membrane in intestinal epithelial cells and transports Pi. In the present study, we analyzed the phenotype of Npt2b -/-and hetero +/-mice. Npt2b -/-mice died in utero soon after implantation, indicating that Npt2b is essential for early embryonic development. At 4 wk of age, Npt2b +/-mice showed hypophosphatemia and low urinary Pi excretion. Plasma fibroblast growth factor 23 levels were significantly decreased and 1,25(OH)2D3 levels were significantly increased in Npt2b +/-mice compared with Npt2b +/+ mice. Npt2b mRNA levels were reduced to 50% that in Npt2b +/+ mice. In contrast, renal Npt2a and Npt2c transporter protein levels were significantly increased in Npt2b +/-mice. At 20 wk of age, Npt2b +/-mice showed hypophosphaturia and reduced Na/P i cotransport activity in the distal intestine. Npt2b +/+ mice with adenine-induced renal failure had hyperphosphatemia and high plasma creatinine levels. Npt2b +/-mice treated with adenine had significantly reduced plasma Pi levels compared with Npt2b +/-mice. Intestinal Npt2b protein and Na +/P i transport activity levels were significantly lower in Npt2b +/-mice than in the Npt2b +/+ mice. The findings of the present studies suggest that Npt2b is an important target for the prevention of hyperphosphatemia. © 2011 the American Physiological Society.

DOI： 10.1152/ajprenal.00663.2010

Scopus

PubMed

Inorganic phosphate homeostasis in sodium-dependent phosphate cotransporter Npt2b⁺/⁻ mice. 査読

American journal of physiology. Renal physiology 301 ( 5 ) F1105 - F1113 2011年11月

Sodium-dependent phosphate cotransporters: lessons from gene knockout and mutation studies. 招待国際誌

Miyamoto K, Haito-Sugino S, Kuwahara S, Ohi A, Nomura K, Ito M, Kuwahata M, Kido S, Tatsumi S, Kaneko I, Segawa H.

J Pharm Sci. 100 ( 9 ) 3719 - 3730 2011年9月

Sodium-Dependent Phosphate Cotransporters: Lessons from Gene Knockout and Mutation Studies 査読

Ken-Ichi Miyamoto, Sakiko Haito-Sugino, Shoji Kuwahara, Akiko Ohi, Kengo Nomura, Mikiko Ito, Masashi Kuwahata, Shinsuke Kido, Sawako Tatsumi, Ichiro Kaneko, Hiroko Segawa

JOURNAL OF PHARMACEUTICAL SCIENCES 100 ( 9 ) 3719 - 3730 2011年9月

記述言語：英語出版者・発行元：WILEY

Inorganic phosphate (Pi) is an essential physiological compound, highlighted by the syndromes caused by hypo or hyperphosphatemic states. Hyperphosphatemia is associated with ectopic calcification, cardiovascular disease, and increased mortality in patients with chronic kidney disease (CKD). As phosphate control is not efficient with diet or dialysis, oral Pi binders are used in over 90% of patients with renal failure. However, achieving tight control of serum Pi is difficult, and lower levels of serum Pi (severe hypophosphatemia) do not lead to better outcomes. The inhibition of sodium-dependent Pi (NaPi) transporter would be a preferable method to control serum Pi levels in patients with CKD or patients undergoing dialysis. Three types of NaPi transporters (types I-III) have been identified: solute carrier series SLC17A1 (NPT1/NaPi-I/OATv1), SLC34 (NaPi-IIa, NaPi-IIb, NaPi-IIc), and SLC20 (PiT1, PiT2), respectively. Knockout mice have been created for types I-III NaPi transporters. In this review, we discuss the roles of the NaPi transporters in Pi homeostasis. (C) 2011 Wiley-Liss, Inc. and the American Pharmacists Association J Pharm Sci 100:3719-3730, 2011

DOI： 10.1002/jps.22614

Web of Science

PubMed

高カルシウム尿を伴う遺伝性低リン血症性クル病の原因遺伝子リン酸トランスポーターNPT2cの変異体解析

塩崎雄治, 杉野さきこ, 大井彰子, 辰巳佐和子, 伊藤美紀子, 宮本賢一

日本腎臓学会誌 53 ( 3 ) 366 - 366 2011年5月

リン代謝における骨細胞の役割

山口誠一, 辰巳佐和子, 釜谷達哉, 塩崎雄治, 野村憲吾, 齋藤友紀子, 木戸慎介, 宮本賢一

腎と骨代謝 23 ( 4 ) 343 - 343 2010年10月

An apical expression signal of the renal type IIc Na+-dependent phosphate cotransporter in renal epithelial cells. 国際誌

Ito M, Sakurai A, Hayashi K, Ohi A, Kangawa N, Nishiyama T, Sugino S, Uehata Y, Kamahara A, Sakata M, Tatsumi S, Kuwahata M, Taketani Y, Segawa H, Miyamoto K.

Am J Physiol Renal Physiol. 299 ( 1 ) F243 - F254 2010年7月

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