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


The Latest on X

Kidney Week

Abstract: SA-PO078

Efficacy of Mesenchymal Stromal Cells in Ameliorating Renal Ischemia/Reperfusion Injury In Vitro

Session Information

  • AKI: Mechanisms - III
    November 05, 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


  • Faria, João, Universiteit Utrecht, Utrecht, Utrecht, Netherlands
  • Calcat-i-Cervera, Sandra, National University of Ireland Galway, Galway, Galway, Ireland
  • Skovronova, Renata, Universita degli Studi di Torino, Torino, Piemonte, Italy
  • Bussolati, Benedetta, Universita degli Studi di Torino, Torino, Piemonte, Italy
  • O'Brien, Timothy, National University of Ireland Galway, Galway, Galway, Ireland
  • Mihaila, Silvia M., Universiteit Utrecht, Utrecht, Utrecht, Netherlands
  • Masereeuw, Rosalinde, Universiteit Utrecht, Utrecht, Utrecht, Netherlands

Renal ischaemia/reperfusion injury (IRI) is the leading cause of acute kidney injury. The current standard of care focuses on treatments to support kidney function, reinforcing the need for more efficient therapies. Mesenchymal stromal cell (MSC) therapy has shown promising results in several preclinical studies. However, their full potential is still unknown.


To mimic ischemia, human conditionally immortalized proximal tubule epithelial cells (ciPTECs) were exposed for 24 hours to a combination of antimycin A (AA) and 2-deoxy glucose (2DG) under hypoxia and normoxia conditions.
Furthermore, ischemic ciPTECs were treated for 24 hours with either conditioned medium (CM) or extracellular vesicles (microvesicles, MV or exosomes, EX) isolated from various sources of MSCs.


When ciPTECs were exposed to ischemic injury (AA and 2DG), actin filaments were lost and nuclei fragmented. In ischemic cells, there was a decrease in metabolic activity (22% in normoxia, 42% in hypoxia; p<0.0001) and ATP production (6% in normoxia, 35% in hypoxia; p<0.001) compared to control cells. In normoxia, the increase in ROS production was more exponential than in hypoxia (p<0.01), and injured cells cultured in hypoxia showed a 75% decrease in mitochondrial mass compared to 20% in normoxia (p<0.0001). The metabolic activity of the injured cells after MSC treatment was similar to that of the injured cells treated with serum (reperfusion group). All cells treated with CM or EVs showed an increase in ATP production of 40-45% (p<0.001) in both normoxia and hypoxia. The Seahorse extracellular flux assay was performed to both injured cells and post-treatment, which revealed a 50% decrease in oxygen consumption rate compared to control cells, that was restored after treatment with either CM from adipose tissue or bone marrow-derived EVs. The extracellular acidification rate, an indicator of a metabolic switch to glycolysis, was reduced by 40% in injured cells and returned to baseline after MSC treatment.


Our findings showed that our in vitro model was capable of replicating in vivo-like morphological and molecular changes observed during IRI. Following MSC treatment, the changes observed in our ischemic cells were moderately reversed, demonstrating MSC's therapeutic potential.


  • Government Support – Non-U.S.