References of "Cytotherapy"
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See detailHuman bone marrow, umbilical cord or liver mesenchymal stromal cells fail to improve liver function in a model of CCl4-induced liver damage in NOD/SCID/IL-2Ry(null) mice
BRIQUET, Alexandra ULg; GREGOIRE, Céline ULg; Comblain, Fanny ULg et al

in Cytotherapy (2014), 16

Background aims. Transplantation is the gold standard procedure for treating acute and chronic end-stage liver diseases. Given the shortage of organs, the development of cellular sources other than human ... [more ▼]

Background aims. Transplantation is the gold standard procedure for treating acute and chronic end-stage liver diseases. Given the shortage of organs, the development of cellular sources other than human liver is urgent. The main objective of this project was to examine the effect of mesenchymal stromal cell (MSC) (bone marrow, umbilical cord and liver MSCs) intravenous injection on liver regeneration in a model of hepatic damage in NOD/SCID/IL non-obese diabetic/severe combined immunodeficient/Interleukin-2Rg(null) (NSG) mice. Methods. Mice received 3 intraperitoneal injections of CCl4 Carbon tetrachloride per week for 4 weeks. Forty-eight hours after the last injection of CCl4, mice received 500,000 MSCs or phosphate-buffered saline by intravenous injection. We examined hepatic damage by means of quantitative image analysis and blood enzyme analysis 24 h, 1 week or 8 weeks after MSC or phosphate-buffered saline injection. We also examined MSC homing by means of real-time polymerase chain reaction of human albumin. Results. We adapted a model of liver injury in immunodeficient mice. In this model, accumulation of collagen in newly formed scar septa was apparent up to 8 weeks after CCl4 treatment. Human albumin DNA was found in all organs tested. However, intravenous MSC injection, even after CXCR4 C-X-C chemokine receptor type 4 transduction and whatever the origin of MSCs, failed to improve liver damage. Conclusions. In this liver injury model, MSCs were propagated in various tissues, particularly filtering organs. For the treatment of hepatic damage, intravenous administration of moderate doses of MSCs does not appear to be effective. Yet, this adapted liver injury model is appropriate for investigating engraftment of human cells. [less ▲]

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See detailImpact of bone marrow-derived mesenchymal stromal cells on experimental xenogeneic graft-versus-host disease
Bruck, France; Belle, Ludovic ULg; LECHANTEUR, Chantal ULg et al

in Cytotherapy (2013), 15(3), 267-279

Background aims. Graft-versus-host disease (GVHD) is a life-threatening complication of allogeneic hematopoietic cell transplantation caused by donor T cells reacting against host tissues. Previous ... [more ▼]

Background aims. Graft-versus-host disease (GVHD) is a life-threatening complication of allogeneic hematopoietic cell transplantation caused by donor T cells reacting against host tissues. Previous studies have suggested that mesenchymal stromal cells (MSCs) could exert potent immunosuppressive effects. Methods. The ability of human bone marrow derived MSCs to prevent xenogeneic GVHD in non-obese diabetic/severe combined immunodeficient (NOD/SCID) mice and in NOD/SCID/interleukin-2Rg(null) (NSG) mice transplanted with human peripheral blood mononuclear cells (PBMCs) was assessed. Results. Injection of 200 106 human PBMCs intraperitoneally (IP) into sub-lethally (3.0 Gy) irradiated NOD/SCID mice also given anti-asialo GM1 antibodies IP 1 day prior and 8 days after transplantation induced lethal xenogeneic GVHD in all tested mice. Co-injection of 2 106 MSCs IP on day 0 did not prevent lethal xenogeneic GVHD induced by injection of human PBMCs. Similarly, injection of 30 106 human PBMCs IP into sub-lethally (2.5 Gy) irradiated NSG mice induced a lethal xenogeneic GVHD in all tested mice. Injection of 3 106 MSCs IP on days 0, 7, 14 and 21 did not prevent lethal xenogeneic GVHD induced by injection of human PBMCs. Conclusions. Injection of MSCs did not prevent xenogeneic GVHD in these two humanized mice models. [less ▲]

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See detailSpontaneous and granulocyte–colony-stimulating factor-enhanced marrow response and progenitor cell mobilization in mice after myocardial infarction.
Delgaudine, Marie ULg; Gothot, André ULg; Beguin, Yves ULg

in Cytotherapy (2010), 12(7), 909-18

BACKGROUND AIMS: Hematopoietic (HPC), mesenchymal (MPC) and/or endothelial (EPC) progenitor cells are being studied to repair the myocardium after acute or chronic ischemia. We examined marrow response to ... [more ▼]

BACKGROUND AIMS: Hematopoietic (HPC), mesenchymal (MPC) and/or endothelial (EPC) progenitor cells are being studied to repair the myocardium after acute or chronic ischemia. We examined marrow response to myocardial infarction (MI) and the ability of granulocyte-colony-stimulating factor (G-CSF) to enhance mobilization of HPC, MPC and EPC in peripheral blood (PB) and bone marrow (BM) of MI mice. METHODS: We induced MI in C57Bl/6 mice, while sham-operated (SO) animals were similarly operated on but without coronary artery ligation. Animals were treated with either saline or G-CSF, from day -5 to day +5 after MI or from day 0 to day +5. Progenitor cell numbers in PB and BM were evaluated by fluorescence-activated cell sorting (FACS) analysis and cell culture. RESULTS: White blood cells (WBC) decreased in BM and increased in PB after MI; G-CSF amplified this effect in BM but not in PB. HPC numbers decreased in BM after MI, while HPC and granulocyte-macrophage colony-forming units (GM-CFU) increased in PB only after G-CSF treatment, and more prominently so in MI than in SO mice. MPC and fibroblast-colony-forming units (F-CFU) as well as EPC were mobilized into the PB after MI and further after G-CSF treatment. Plasma troponin T concentrations decreased after G-CSF treatment. CONCLUSIONS: BM is globally affected by acute MI, but not simple body injury, with intense mobilization of marrow MPC and EPC into the PB but inhibition of HPC. Progenitor cell entry into the PB may be paralleled by depletion of their BM pools. G-CSF is required for HPC mobilization and enhances MPC and EPC entry into the PB. [less ▲]

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