Publications by authors named "Marie Goulard"

7 Publications

  • Page 1 of 1

Modulating endothelial cells with EGFL7 to diminish aGVHD after allogeneic bone marrow transplantation in mice.

Blood Adv 2021 Oct 15. Epub 2021 Oct 15.

Hopital Maisonneuve-Rosemont, Canada.

Acute graft versus host (aGVHD) is the second cause of death after allogeneic-hematopoietic stem cell transplant (allo-HSCT) underscoring the need for novel therapies. Based on previous work that endothelial cell dysfunction is present in aGVHD and that epidermal growth factor-like domain 7 (EGFL7) plays a significant role in decreasing inflammation by repressing endothelial cell activation and T cell migration, we hypothesized that increasing EGFL7 levels after allo-HSCT will diminish the severity of aGVHD. Here, we show that treatment with recombinant EGFL7 (rEGFL7) in two different murine models of aGVHD decreases aGVHD severity and improves survival in recipient mice after allogeneic transplantation with respect to controls without affecting graft versus leukemia effect. Furthermore, we showed that rEGFL7 treatment results in higher thymocytes, T, B and dendritic cells in recipient mice after allo-HSCT. This study constitutes a proof of concept of the ability of rEGFL7 therapy to reduce GHVD severity and mortality after allo-HSCT.
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http://dx.doi.org/10.1182/bloodadvances.2021005498DOI Listing
October 2021

Analysis of Hematopoietic Stem Progenitor Cell Metabolism.

J Vis Exp 2019 11 9(153). Epub 2019 Nov 9.

Nationwide Children's Hospital; The Ohio State University College of Medicine; The Ohio State University Comprehensive Cancer Center;

Hematopoietic stem progenitor cells (HSPCs) have distinct metabolic plasticity, which allows them to transition from their quiescent state to a differentiation state to sustain demands of the blood formation. However, it has been difficult to analyze the metabolic status (mitochondrial respiration and glycolysis) of HSPCs due to their limited numbers and lack of optimized protocols for non-adherent, fragile HSPCs. Here, we provide a set of clear, step-by-step instructions to measure metabolic respiration (oxygen consumption rate; OCR) and glycolysis (extracellular acidification rate; ECAR) of murine bone marrow-LineageSca1c-Kit (LSK) HSPCs. This protocol provides a higher amount of LSK HSPCs from murine bone marrow, improves the viability of HSPCs during incubation, facilitates extracellular flux analyses of non-adherent HSPCs, and provides optimized injection protocols (concentration and time) for drugs targeting oxidative phosphorylation and glycolytic pathways. This method enables the prediction of the metabolic status and the health of HSPCs during blood development and diseases.
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http://dx.doi.org/10.3791/60234DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6897312PMC
November 2019

Directed Collective Cell Migration Using Three-Dimensional Bioprinted Micropatterns on Thermoresponsive Surfaces for Myotube Formation.

ACS Biomater Sci Eng 2019 08 6;5(8):3935-3943. Epub 2019 Feb 6.

Center for Childhood Cancers and Blood Diseases, Nationwide Children's Hospital, Columbus, Ohio 43205, United States.

Directed collective cell migration governs cell orientation during tissue morphogenesis, wound healing, and tumor metastasis. Unfortunately, current methods for initiating collective cell migration, such as scratching, laser ablation, and stencils, either introduce uncontrolled cell-injury, involve multiple fabrication processes, or have utility limited to cells with strong cell-cell junctions. Using three-dimensional (3D) bioprinted gelatin methacryloyl (GelMA) micropatterns on temperature-responsive poly(-isopropylacrylamide) (PNIPAm) coated interfaces, we demonstrate that directed injury-free collective cell migration could occur in parallel and perpendicular directions. After seeding cells, we created cell-free spaces between two 3D bioprinted GelMA micropatterns by lowering the temperature of PNIPAm interfaces to promote the cell detachment. Unlike conventional collective cell migration methods initiated by stencils, we observed well-organized cell migration in parallel and perpendicular to 3D bioprinted micropatterns as a function of the distance between 3D bioprinted micropatterns. We further established the utility of controlled collective cell migration for directed functional myotube formation using 3D bioprinted fingerprintlike micropatterns as well as iris musclelike concentric circular patterns. Our platform is unique for myoblast alignment and myotube formation because it does not require anisotropic guidance cues. Together, our findings establish how to achieve controlled collective cell migration, even at the macroscale, for tissue engineering and regeneration.
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http://dx.doi.org/10.1021/acsbiomaterials.8b01359DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6853623PMC
August 2019

[Towards a personalized pretransplantation conditioning in patients with myelodysplastic syndromes].

Med Sci (Paris) 2018 Jan 31;34(1):9-11. Epub 2018 Jan 31.

Inserm UMR-S-1131, 1, avenue Claude Vellefaux, 75010 Paris, France - APHP, Hôpital Saint-Louis, unité de biologie cellulaire, 1, avenue Claude Vellefaux, 75010 Paris, France.

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http://dx.doi.org/10.1051/medsci/20183401002DOI Listing
January 2018

Role of the microenvironment in myeloid malignancies.

Cell Mol Life Sci 2018 Apr 8;75(8):1377-1391. Epub 2017 Dec 8.

Haematopoietic Stem Cell Laboratory, The Francis Crick Institute, 1, Midland Road, London, NW1 1AT, UK.

The bone marrow microenvironment (BMM) regulates the fate of hematopoietic stem cells (HSCs) in homeostatic and pathologic conditions. In myeloid malignancies, new insights into the role of the BMM and its cellular and molecular actors in the progression of the diseases have started to emerge. In this review, we will focus on describing the major players of the HSC niche and the role of the altered niche function in myeloid malignancies, more specifically focusing on the mesenchymal stroma cell compartment.
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http://dx.doi.org/10.1007/s00018-017-2725-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5852194PMC
April 2018

Stability of preclinical models of aggressive renal cell carcinomas.

Int J Clin Exp Pathol 2014 15;7(6):2950-62. Epub 2014 May 15.

Université Paris Diderot, Sorbonne Paris Cité F-75010 Paris, France ; INSERM, U1165 Paris, F-75010 France ; AP-HP-Hôpital Saint-Louis, Laboratoire de Pathologie Paris, F-75010 France.

Renal-cell carcinomas (RCC) are often resistant to conventional cytotoxic agents. Xenograft models are used for in vivo preclinical studies and drug development. The validity of these studies is highly dependent on the phenotypic and genotypic stability of the models. Here we assessed the stability of six aggressive human RCC xenografted in nude/NMRI mice. We compared the initial samples (P0), first (P1) and fifth (P5) passages for the following criteria: histopathology, immunohistochemistry for CK7, CD10, vimentin and p53, DNA allelic profiles using 10 microsatellites and CGH-array. Next we evaluated the response to sunitinib in primary RCC and corresponding xenografted RCC. We observed a good overall stability between primary RCC and corresponding xenografted RCC at P1 and P5 regarding histopathology and immunohistochemistry except for cytokeratin 7 (one case) and p53 (one case) expression. Out of 44 groups with fully available microsatellite data (at P0, P1 and P5), 66% (29 groups) showed no difference from P0 to P5 while 34% (15 groups) showed new or lost alleles. Using CGH-array, overall genomic alterations at P5 were not different from those of initial RCC. The xenografted RCC had identical response to sunitinib therapy compared to the initial human RCC from which they derive. These xenograft models of aggressive human RCC are clinically relevant, showing a good histological and molecular stability and are suitable for studies of basic biology and response to therapy.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4097235PMC
May 2015

Lithium enhances remyelination of peripheral nerves.

Proc Natl Acad Sci U S A 2012 Mar 21;109(10):3973-8. Epub 2012 Feb 21.

Unité Mixte de Recherche 8194, Centre National de la Recherche Scientifique, University Paris Descartes, 75270 Paris Cedex 06, France.

Glycogen synthase kinase 3β (GSK3β) inhibitors, especially the mood stabilizer lithium chloride, are also used as neuroprotective or anti-inflammatory agents. We studied the influence of LiCl on the remyelination of peripheral nerves. We showed that the treatment of adult mice with LiCl after facial nerve crush injury stimulated the expression of myelin genes, restored the myelin structure, and accelerated the recovery of whisker movements. LiCl treatment also promoted remyelination of the sciatic nerve after crush. We also demonstrated that peripheral myelin gene MPZ and PMP22 promoter activities, transcripts, and protein levels are stimulated by GSK3β inhibitors (LiCl and SB216763) in Schwann cells as well as in sciatic and facial nerves. LiCl exerts its action in Schwann cells by increasing the amount of β-catenin and provoking its nuclear localization. We showed by ChIP experiments that LiCl treatment drives β-catenin to bind to T-cell factor/lymphoid-enhancer factor response elements identified in myelin genes. Taken together, our findings open perspectives in the treatment of nerve demyelination by administering GSK3β inhibitors such as lithium.
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http://dx.doi.org/10.1073/pnas.1121367109DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3309729PMC
March 2012
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