ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2023 and some content may be unavailable. To unlock all content for 2023, please visit the archives.

Abstract: SA-PO349

Urine-Derived Stem Cell Administration Attenuates Renal Injury in an Adriamycin-Induced Nephropathy

Session Information

Category: Development, Stem Cells, and Regenerative Medicine

  • 600 Development, Stem Cells, and Regenerative Medicine

Authors

  • Park, Kyungho, Chungnam National University Hospital, Daejeon, Korea (the Republic of)
  • Park, Heewon, Chungnam National University Hospital, Daejeon, Korea (the Republic of)
  • Hwang, Yunkyeong, Chungnam National University Hospital, Daejeon, Korea (the Republic of)
  • Han, Suyeon, Chungnam National University Hospital, Daejeon, Korea (the Republic of)
  • Park, Hye Rim, Department of Medical Science, Chungnam National University, Daejeon, Korea (the Republic of)
  • Lee, Eu Jin, Chungnam National University Hospital, Daejeon, Korea (the Republic of)
  • Kim, Hae Ri, Chungnam National University Sejong Hospital, Sejong, Korea (the Republic of)
  • Ham, Youngrok, Chungnam National University Hospital, Daejeon, Korea (the Republic of)
  • Na, Kiryang, Chungnam National University Hospital, Daejeon, Korea (the Republic of)
  • Lee, Kang Wook, Chungnam National University Hospital, Daejeon, Korea (the Republic of)
  • Choi, Dae Eun, Chungnam National University Hospital, Daejeon, Korea (the Republic of)
Background

Stem cell-based therapy as a potential alternative to conventional drug therapies for kidney diseases has attracted significant attention. While mesenchymal stem cells have been extensively studied in early clinical trials for various kidney diseases, research on urine-derived stem cells (UDSCs) remains limited. This study aims to evaluate the efficacy of UDSC administration in improving Adriamycin (ADR)-nephropathy using both an in vivo BALB/c mice model and an in vitro podocyte model.

Methods

10 week-old male BALB/c mice were divided into four groups: sham, ADR, ADR+HS (single dose of UDSC), ADR+HM (three doses of UDSC) to establish the in vivo model. ADR was administered on day 0, followed by UDSC administration one week later. Necropsy and analysis were conducted on the 21st day. The urine albumin/creatinine ratio (ACR) was measured on days 0, 7, 14, and 21, and kidney tissue was examined using light microscopy, immunofluorescence microscopy, and electron microscopy. In vitro, the protective effect of UDSC co-culture with ADR-treated podocytes was investigated through cell viability assessment and the expression of podocyte-specific markers, such as α-actinin-4 and synaptopodin.

Results

Both single-dose (ADR+HS) and multiple-dose (ADR+HM) UDSC administration significantly reduced the urine ACR levels compared to the ADR group. Histological analysis revealed notable improvements in renal tissue damage, including glomerulosclerosis and fibrosis, in both the ADR+HS and ADR+HM groups compared to the ADR group. Moreover, UDSC administration protected podocytes from damage, as indicated by increased foot process width. UDSC administration also enhanced expression of synaptopodin and α-actinin-4. Notably, ADR+HM showed a more pronounced effect on foot process width increase and improvement in the expression of α-actinin-4 and synaptopodin in podocytes compared ADR+HS. In vitro model, co-culture with UDSC significantly enhanced podocyte cell viability compared to ADR-treated podocytes alone. Furthermore, co-culture with UDSCs led to a significant increase in the expression of α-actinin-4 and synaptopodin in ADR-treated podocytes.

Conclusion

Administration of UDSCs demonstrates significant reduction in kidney damage in both in vivo and in vitro models of ADR-induced nephropathy.