Risedronate Attenuates Podocyte Injury in Phosphate Transporter-Overexpressing Rats

Yohei Asada, Takeshi Takayanagi, Tsukasa Kawakami, Eisuke Tomatsu, Atsushi Masuda, Yasumasa Yoshino, Sahoko Sekiguchi-Ueda, Megumi Shibata, Tomihiko Ide, Hajime Niimi, Eishin Yaoita, Yusuke Seino, Yoshihisa Sugimura, Atsushi Suzuki

研究成果: Article

抄録

Osteoporosis patients with chronic kidney disease (CKD) are becoming common in our superaging society. Renal dysfunction causes phosphorus accumulation in the circulating plasma and leads to the development of CKD-mineral bone disorder (MBD). We have previously reported that type III Pi transporter-overexpressing transgenic (Pit-1 TG) rats manifest phosphate (Pi)-dependent podocyte injury. In the present study, we explored the effect of risedronate on Pi-induced podocyte injury in vivo. Pit-1 TG rats and wild-type rats at 5 weeks old were divided into a risedronate-treated group and an untreated group. We subcutaneously administered 5 μg/kg body weight of risedronate or saline twice a week during the experimental period. Risedronate did not alter serum creatinine levels at 5, 8, and 12 weeks of age. However, electron microscopy images showed that thickening of the glomerular basement membrane was improved in the risedronate treatment group. Furthermore, immunostaining for podocyte injury markers revealed that both desmin- and connexin43-positive areas were smaller in the risedronate-treated group than in the untreated group, suggesting that bisphosphonates could rescue Pi-induced podocyte injury. In conclusion, our findings suggest that risedronate could maintain glomerular barrier function by rescuing Pi-induced podocyte injury.

元の言語English
記事番号4194853
ジャーナルInternational Journal of Endocrinology
2019
DOI
出版物ステータスPublished - 01-01-2019

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Phosphate Transport Proteins
Podocytes
Wounds and Injuries
Chronic Kidney Disease-Mineral and Bone Disorder
Glomerular Basement Membrane
Connexin 43
Desmin
Diphosphonates
Risedronate Sodium
Chronic Renal Insufficiency
Phosphorus
Osteoporosis
Creatinine
Electron Microscopy
Phosphates
Body Weight
Kidney

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology
  • Endocrine and Autonomic Systems

これを引用

Asada, Yohei ; Takayanagi, Takeshi ; Kawakami, Tsukasa ; Tomatsu, Eisuke ; Masuda, Atsushi ; Yoshino, Yasumasa ; Sekiguchi-Ueda, Sahoko ; Shibata, Megumi ; Ide, Tomihiko ; Niimi, Hajime ; Yaoita, Eishin ; Seino, Yusuke ; Sugimura, Yoshihisa ; Suzuki, Atsushi. / Risedronate Attenuates Podocyte Injury in Phosphate Transporter-Overexpressing Rats. :: International Journal of Endocrinology. 2019 ; 巻 2019.
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title = "Risedronate Attenuates Podocyte Injury in Phosphate Transporter-Overexpressing Rats",
abstract = "Osteoporosis patients with chronic kidney disease (CKD) are becoming common in our superaging society. Renal dysfunction causes phosphorus accumulation in the circulating plasma and leads to the development of CKD-mineral bone disorder (MBD). We have previously reported that type III Pi transporter-overexpressing transgenic (Pit-1 TG) rats manifest phosphate (Pi)-dependent podocyte injury. In the present study, we explored the effect of risedronate on Pi-induced podocyte injury in vivo. Pit-1 TG rats and wild-type rats at 5 weeks old were divided into a risedronate-treated group and an untreated group. We subcutaneously administered 5 μg/kg body weight of risedronate or saline twice a week during the experimental period. Risedronate did not alter serum creatinine levels at 5, 8, and 12 weeks of age. However, electron microscopy images showed that thickening of the glomerular basement membrane was improved in the risedronate treatment group. Furthermore, immunostaining for podocyte injury markers revealed that both desmin- and connexin43-positive areas were smaller in the risedronate-treated group than in the untreated group, suggesting that bisphosphonates could rescue Pi-induced podocyte injury. In conclusion, our findings suggest that risedronate could maintain glomerular barrier function by rescuing Pi-induced podocyte injury.",
author = "Yohei Asada and Takeshi Takayanagi and Tsukasa Kawakami and Eisuke Tomatsu and Atsushi Masuda and Yasumasa Yoshino and Sahoko Sekiguchi-Ueda and Megumi Shibata and Tomihiko Ide and Hajime Niimi and Eishin Yaoita and Yusuke Seino and Yoshihisa Sugimura and Atsushi Suzuki",
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Asada, Y, Takayanagi, T, Kawakami, T, Tomatsu, E, Masuda, A, Yoshino, Y, Sekiguchi-Ueda, S, Shibata, M, Ide, T, Niimi, H, Yaoita, E, Seino, Y, Sugimura, Y & Suzuki, A 2019, 'Risedronate Attenuates Podocyte Injury in Phosphate Transporter-Overexpressing Rats', International Journal of Endocrinology, 巻. 2019, 4194853. https://doi.org/10.1155/2019/4194853

Risedronate Attenuates Podocyte Injury in Phosphate Transporter-Overexpressing Rats. / Asada, Yohei; Takayanagi, Takeshi; Kawakami, Tsukasa; Tomatsu, Eisuke; Masuda, Atsushi; Yoshino, Yasumasa; Sekiguchi-Ueda, Sahoko; Shibata, Megumi; Ide, Tomihiko; Niimi, Hajime; Yaoita, Eishin; Seino, Yusuke; Sugimura, Yoshihisa; Suzuki, Atsushi.

:: International Journal of Endocrinology, 巻 2019, 4194853, 01.01.2019.

研究成果: Article

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T1 - Risedronate Attenuates Podocyte Injury in Phosphate Transporter-Overexpressing Rats

AU - Asada, Yohei

AU - Takayanagi, Takeshi

AU - Kawakami, Tsukasa

AU - Tomatsu, Eisuke

AU - Masuda, Atsushi

AU - Yoshino, Yasumasa

AU - Sekiguchi-Ueda, Sahoko

AU - Shibata, Megumi

AU - Ide, Tomihiko

AU - Niimi, Hajime

AU - Yaoita, Eishin

AU - Seino, Yusuke

AU - Sugimura, Yoshihisa

AU - Suzuki, Atsushi

PY - 2019/1/1

Y1 - 2019/1/1

N2 - Osteoporosis patients with chronic kidney disease (CKD) are becoming common in our superaging society. Renal dysfunction causes phosphorus accumulation in the circulating plasma and leads to the development of CKD-mineral bone disorder (MBD). We have previously reported that type III Pi transporter-overexpressing transgenic (Pit-1 TG) rats manifest phosphate (Pi)-dependent podocyte injury. In the present study, we explored the effect of risedronate on Pi-induced podocyte injury in vivo. Pit-1 TG rats and wild-type rats at 5 weeks old were divided into a risedronate-treated group and an untreated group. We subcutaneously administered 5 μg/kg body weight of risedronate or saline twice a week during the experimental period. Risedronate did not alter serum creatinine levels at 5, 8, and 12 weeks of age. However, electron microscopy images showed that thickening of the glomerular basement membrane was improved in the risedronate treatment group. Furthermore, immunostaining for podocyte injury markers revealed that both desmin- and connexin43-positive areas were smaller in the risedronate-treated group than in the untreated group, suggesting that bisphosphonates could rescue Pi-induced podocyte injury. In conclusion, our findings suggest that risedronate could maintain glomerular barrier function by rescuing Pi-induced podocyte injury.

AB - Osteoporosis patients with chronic kidney disease (CKD) are becoming common in our superaging society. Renal dysfunction causes phosphorus accumulation in the circulating plasma and leads to the development of CKD-mineral bone disorder (MBD). We have previously reported that type III Pi transporter-overexpressing transgenic (Pit-1 TG) rats manifest phosphate (Pi)-dependent podocyte injury. In the present study, we explored the effect of risedronate on Pi-induced podocyte injury in vivo. Pit-1 TG rats and wild-type rats at 5 weeks old were divided into a risedronate-treated group and an untreated group. We subcutaneously administered 5 μg/kg body weight of risedronate or saline twice a week during the experimental period. Risedronate did not alter serum creatinine levels at 5, 8, and 12 weeks of age. However, electron microscopy images showed that thickening of the glomerular basement membrane was improved in the risedronate treatment group. Furthermore, immunostaining for podocyte injury markers revealed that both desmin- and connexin43-positive areas were smaller in the risedronate-treated group than in the untreated group, suggesting that bisphosphonates could rescue Pi-induced podocyte injury. In conclusion, our findings suggest that risedronate could maintain glomerular barrier function by rescuing Pi-induced podocyte injury.

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Asada Y, Takayanagi T, Kawakami T, Tomatsu E, Masuda A, Yoshino Y その他. Risedronate Attenuates Podocyte Injury in Phosphate Transporter-Overexpressing Rats. International Journal of Endocrinology. 2019 1 1;2019. 4194853. https://doi.org/10.1155/2019/4194853