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 Twitter

Kidney Week

Abstract: TH-PO654

Differentiation Efficiency of Human Induced Pluripotent Stem Cell (iPSC) to Endothelial Cells in Patients with ESRD

Session Information

Category: Development, Stem Cells, and Regenerative Medicine

  • 502 Development, Stem Cells, and Regenerative Medicine: Clinical

Author

  • Na, Do-hyun, St. Mary's Hospital, College of Medicine, Seoul, Korea (the Republic of)

Group or Team Name

  • Transplant research center, St. Mary's Hospital, College of Medicine
Background

Human induced pluripotent stem cell-derived endothelial cells (hiPSC-ECs) could be promising for treatment of renal disease. However, it is unclear whether hiPSC could be differentiated to endothelial cell (EC) in ESRD patients. Therefore, we first sought to generate hiPSC from peripheral blood mononuclear cell (PBMC) of ESRD patient, then compared the efficiency of hiPSC lines differentiating into ECs with healthy control.

Methods

The hiPSC-ECs were generated from differentiation of hiPSCs using vascular endothelial growth factor (VEGF) and bone morphogenetic protein-4 (BMP-4). At first, the expression of iPSC markers (NANOG, SSEA-4, and TRA-1-81) were assessed with confocal laser scanning microscopy, then hiPSC-ECs were purified based on positive expression of CD31. Subsequently, expression of endothelial markers (CD31, CD 34, and CD 133) were assessed with flow cytometric analysis. After 6 days in cell culture, stain with pluripotency markers (NANOG, SSEA-4, and TRA-1-81) on confocal image revealed iPSC were successfully generated in both healthy control and ESRD patient.

Results

Upon magnetic purification based on CD31+ expression, the hiPSC-EC population was observed to display typical endothelial surface markers in both groups (CD31, CD34, CD133, vWF, and Flt). However, hiPSC-ECs from ESRD patient showed much lower colonies of co-expression of CD31/CD34, CD31/CD133, and CD34/CD133 in FACS, compared to normal control. This was consistent with that the percentage of CD31 expression cell or co-expression of CD31/CD34 cells to total cells were much lower in ESRD group compared to that of healthy control.

Conclusion

In conclusion, the efficiency of hiPSC differentiating into ECs in ESRD patient were diminished compared to healthy control.