Autologous cell therapy for cisplatin-induced acute kidney injury by using non-expanded adipose tissue-derived cells

Kaoru Yasuda, Takenori Ozaki, Yousuke Saka, Tokunori Yamamoto, Momokazu Gotoh, Yasuhiko Ito, Yukio Yuzawa, Seiichi Matsuo, Shoichi Maruyama

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

Background aims. Recent studies have demonstrated that cultured mesenchymal stromal cells derived from adipose tissue are useful for regenerative cell therapy. The stromal vascular fraction (SVF) can be obtained readily without culturing and may be clinically applicable. We investigated the therapeutic effects of SVF and used it in the treatment of acute kidney injury (AKI). Methods. Liposuction aspirates were obtained from healthy donors who had provided written informed consent. We harvested the SVF and determined the growth factor secretion and anti-apoptotic ability with conditioned medium. To investigate the effect of SVF on AKI, cisplatin was injected into rats and SVF was administrated into the subcupsula of the kidney. Results. Both human and rat SVF cells secreted vascular endothelial growth factor-A (VEGF) and hepatocyte growth factor (HGF). Human SVF-conditioned media had an anti-apoptotic effect, which was inhibited by anti-HGF antibody (Ab) but not by anti-VEGF Ab. In vivo, SVF significantly ameliorated renal function, attenuated tubular damage and increased the cortical blood flow speed. In the SVF-treated group, VEGF levels in the cortex and HGF levels in both the cortex and medulla, especially tubules in the medulla, were significantly higher. Immunostaining revealed that SVF cells expressing VEGF and HGF and remained in the subcapsule on day 14. Conclusions. The present study demonstrates that a subcapsular injection of non-expanded SVF cells ameliorates rat AKI, and that the mechanism probably involves secretion of renoprotective molecules. Administration of human SVF may be clinically applicable and useful as a novel autologous cell therapy against kidney diseases.

Original languageEnglish
Pages (from-to)1089-1100
Number of pages12
JournalCytotherapy
Volume14
Issue number9
DOIs
Publication statusPublished - 01-01-2012
Externally publishedYes

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Cell- and Tissue-Based Therapy
Acute Kidney Injury
Cisplatin
Blood Vessels
Adipose Tissue
Hepatocyte Growth Factor
Vascular Endothelial Growth Factor A
Conditioned Culture Medium
Kidney
Lipectomy
Kidney Diseases
Therapeutic Uses
Informed Consent
Mesenchymal Stromal Cells
Anti-Idiotypic Antibodies
Intercellular Signaling Peptides and Proteins

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology
  • Oncology
  • Genetics(clinical)
  • Cell Biology
  • Transplantation
  • Cancer Research

Cite this

Yasuda, K., Ozaki, T., Saka, Y., Yamamoto, T., Gotoh, M., Ito, Y., ... Maruyama, S. (2012). Autologous cell therapy for cisplatin-induced acute kidney injury by using non-expanded adipose tissue-derived cells. Cytotherapy, 14(9), 1089-1100. https://doi.org/10.3109/14653249.2012.693157
Yasuda, Kaoru ; Ozaki, Takenori ; Saka, Yousuke ; Yamamoto, Tokunori ; Gotoh, Momokazu ; Ito, Yasuhiko ; Yuzawa, Yukio ; Matsuo, Seiichi ; Maruyama, Shoichi. / Autologous cell therapy for cisplatin-induced acute kidney injury by using non-expanded adipose tissue-derived cells. In: Cytotherapy. 2012 ; Vol. 14, No. 9. pp. 1089-1100.
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Yasuda, K, Ozaki, T, Saka, Y, Yamamoto, T, Gotoh, M, Ito, Y, Yuzawa, Y, Matsuo, S & Maruyama, S 2012, 'Autologous cell therapy for cisplatin-induced acute kidney injury by using non-expanded adipose tissue-derived cells', Cytotherapy, vol. 14, no. 9, pp. 1089-1100. https://doi.org/10.3109/14653249.2012.693157

Autologous cell therapy for cisplatin-induced acute kidney injury by using non-expanded adipose tissue-derived cells. / Yasuda, Kaoru; Ozaki, Takenori; Saka, Yousuke; Yamamoto, Tokunori; Gotoh, Momokazu; Ito, Yasuhiko; Yuzawa, Yukio; Matsuo, Seiichi; Maruyama, Shoichi.

In: Cytotherapy, Vol. 14, No. 9, 01.01.2012, p. 1089-1100.

Research output: Contribution to journalArticle

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T1 - Autologous cell therapy for cisplatin-induced acute kidney injury by using non-expanded adipose tissue-derived cells

AU - Yasuda, Kaoru

AU - Ozaki, Takenori

AU - Saka, Yousuke

AU - Yamamoto, Tokunori

AU - Gotoh, Momokazu

AU - Ito, Yasuhiko

AU - Yuzawa, Yukio

AU - Matsuo, Seiichi

AU - Maruyama, Shoichi

PY - 2012/1/1

Y1 - 2012/1/1

N2 - Background aims. Recent studies have demonstrated that cultured mesenchymal stromal cells derived from adipose tissue are useful for regenerative cell therapy. The stromal vascular fraction (SVF) can be obtained readily without culturing and may be clinically applicable. We investigated the therapeutic effects of SVF and used it in the treatment of acute kidney injury (AKI). Methods. Liposuction aspirates were obtained from healthy donors who had provided written informed consent. We harvested the SVF and determined the growth factor secretion and anti-apoptotic ability with conditioned medium. To investigate the effect of SVF on AKI, cisplatin was injected into rats and SVF was administrated into the subcupsula of the kidney. Results. Both human and rat SVF cells secreted vascular endothelial growth factor-A (VEGF) and hepatocyte growth factor (HGF). Human SVF-conditioned media had an anti-apoptotic effect, which was inhibited by anti-HGF antibody (Ab) but not by anti-VEGF Ab. In vivo, SVF significantly ameliorated renal function, attenuated tubular damage and increased the cortical blood flow speed. In the SVF-treated group, VEGF levels in the cortex and HGF levels in both the cortex and medulla, especially tubules in the medulla, were significantly higher. Immunostaining revealed that SVF cells expressing VEGF and HGF and remained in the subcapsule on day 14. Conclusions. The present study demonstrates that a subcapsular injection of non-expanded SVF cells ameliorates rat AKI, and that the mechanism probably involves secretion of renoprotective molecules. Administration of human SVF may be clinically applicable and useful as a novel autologous cell therapy against kidney diseases.

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