Related Experiment Video
Updated: Jul 10, 2026

Stem Cell Transplantation in an in vitro Simulated Ischemia/Reperfusion Model
Published on: November 5, 2011
Evaluation of stem cell administration in a model of kidney ischemia-reperfusion injury
Léa Bueno Lucas da Silva1, Patrícia Viana Bonini Palma, Patrícia Maluf Cury
1Pathology Division, Medical School in São José do Rio Preto FAMERP, São José do Rio Preto, Brazil.
Abstract:
Ischemia-reperfusion injury is a common early event in kidney transplantation and contributes to a delay in organ function. Acute tubular necrosis, impaired kidney function and organ leukocyte infiltration are the major findings. The therapeutic potential of stem cells has been the focus of recent research as these cells possess capabilities such as self-renewal, multipotent differentiation and aid in regeneration after organ injury. FTY720 is a new synthetic compound that has been associated with preferential migration of blood lymphocytes to peripheral lymph nodes instead of inflammatory sites. Bone marrow stem cells (BMSC) and/or FTY720 were used as therapy to promote recovery of tubule cells and avoid inflammation at the renal site, respectively. Mice were submitted to renal ischemia-reperfusion injury and were either treated with two doses of FTY720, 10x10(6) BMSC, or both in order to compare the therapeutic effect with non-treated and control animals. Renal function and structure were investigated as were cell numbers in peripheral blood and spleen. Activation and apoptosis markers were also evaluated in splenocytes using flow cytometry. We found that the combined therapy (FTY720+BMSC) was associated with more significant changes in renal function and structure after ischemia-reperfusion injury when compared with the other groups. Also a decrease at cell numbers and prevention of spleen cells activation and apoptosis was observed. In conclusion, in our model it was not possible to demonstrate the potential of stem cells alone or in combination with FTY720 to promote early kidney recovery after ischemia-reperfusion injury.
Insights
Combined therapy with FTY720 and bone marrow stem cells (BMSC) showed potential in improving kidney function after ischemia-reperfusion injury. However, this study could not demonstrate significant early kidney recovery with stem cells alone or combined with FTY720.
Area of Science:
- Nephrology
- Regenerative Medicine
- Immunology
Background:
- Ischemia-reperfusion injury (IRI) is a major cause of delayed kidney function after transplantation.
- Acute tubular necrosis and leukocyte infiltration are key pathological features of IRI.
- Stem cells and FTY720 are being investigated for their therapeutic potential in organ injury and inflammation.
Purpose of the Study:
- To evaluate the therapeutic effects of bone marrow stem cells (BMSC) and FTY720, alone or in combination, on kidney recovery after IRI.
- To assess the impact of these therapies on renal function, structure, and inflammatory markers.
- To investigate the effects on immune cell populations and activation in spleen and blood.
Main Methods:
- Mice underwent renal ischemia-reperfusion injury and were treated with FTY720, BMSC, or both.
- Renal function and structure were assessed.
- Cell numbers in peripheral blood and spleen were analyzed.
- Splenocyte activation and apoptosis were evaluated using flow cytometry.
Main Results:
- Combined FTY720+BMSC therapy showed more significant improvements in renal function and structure compared to other groups.
- A decrease in cell numbers and prevention of spleen cell activation and apoptosis were observed with combined therapy.
- Stem cells alone or with FTY720 did not demonstrate significant early kidney recovery in this model.
Conclusions:
- The combination of FTY720 and BMSC demonstrated a positive impact on renal recovery post-IRI in mice.
- The study did not confirm the efficacy of stem cells alone or with FTY720 for early kidney recovery after IRI.
- Further research is needed to fully elucidate the therapeutic potential of these agents in kidney transplantation.

