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Abstract: TH-PO109

Adipose-Derived Mesenchymal Stem Cells Cultured in Serum-Free Medium Attenuate Acute Contrast-Induced Nephropathy by Exerting Anti-Apoptotic Effects

Session Information

  • AKI: Mechanisms - I
    November 03, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
    Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms

Authors

  • Kadono, Mitsuki, Hiroshima Daigaku Byoin, Hiroshima, Hiroshima, Japan
  • Ishiuchi, Naoki, Hiroshima Daigaku Byoin, Hiroshima, Hiroshima, Japan
  • Nakashima, Ayumu, Hiroshima Daigaku Byoin, Hiroshima, Hiroshima, Japan
  • Sasaki, Kensuke, Hiroshima Daigaku Byoin, Hiroshima, Hiroshima, Japan
  • Masaki, Takao, Hiroshima Daigaku Byoin, Hiroshima, Hiroshima, Japan
Background

Contrast-induced nephropathy (CIN) is a major clinical problem associated with acute kidney injury during hospitalization, however therapeutic methods for CIN have made little progress. We previously showed that culturing mesenchymal stem cells (MSCs) in serum-free medium enhanced their anti-inflammatory effects. In this study, we investigated the therapeutic effects of human adipose-derived MSCs cultured in serum-free medium (SF-MSCs) on a mouse model of CIN.

Methods

C57BL/6 mice (8 weeks of age) underwent right nephrectomy. One week later, the left renal artery was clamped for 30 min to cause ischemia-reperfusion injury, and mice were injected with iohexol using a retro-orbital injection method. The bodies of mice were shielded using a lead plate, except for the left kidney, which received 10 Gy of X-ray irradiation. MSCs cultured in Dulbecco’s Modified Eagle Medium containing 10% fetal bovine serum (S-MSCs) or SF-MSCs were then injected through the tail vein. We also investigated the ability of conditioned medium from S-MSCs or SF-MSCs to suppress apoptosis of X-ray-irradiated HEK293 cells.

Results

Serum creatinine and blood urea nitrogen levels were remarkably increased in CIN mice injected with phosphate-buffered saline (control), but suppressed in CIN mice injected with SF-MSCs compared with S-MSCs. Similarly, cleaved caspase 3 protein levels and numbers of TUNEL-positive cells were increased in CIN mice, but suppressed in CIN mice injected with SF-MSCs compared with S-MSCs. In addition, protein levels of γH2AX, a marker of chromosomal damage, were upregulated in CIN mice, but reduced by S-MSCs treatment and further reduced by SF-MSCs. In vitro experiments showed that the increase in cleaved caspase 3 protein level induced by radiation of HEK293 cells was more strongly suppressed by conditioned medium from SF-MSCs compared with that from S-MSCs.

Conclusion

Adipose-derived SF-MSCs attenuate CIN by exerting anti-apoptotic effects, indicating that SF-MSCs may be a potential therapy for CIN.