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3. Hypoxia Regulates CD9 Expression and Migration of Lymphoblasts in Childhood B Acute Lymphoblastic Leukemia

Author

Gaudichon, J., Cousin, E., Jakobczyk, H., Debaize, L., Rio, A. G., Arnaud, M. P., Villacreces, A., Praloran, V., Galibert, M. D., Troadec, M. B., Gandemer, V., CHU Caen, Normandie Université (NU)-Tumorothèque de Caen Basse-Normandie (TCBN), Institut de Génétique et Développement de Rennes (IGDR), Université de Rennes (UR)-Centre National de la Recherche Scientifique (CNRS)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), Biothérapies des maladies génétiques et cancers, Université Bordeaux Segalen - Bordeaux 2-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Brest (UBO), CHU Pontchaillou [Rennes], Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )-Centre National de la Recherche Scientifique (CNRS)-Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES), and Jonchère, Laurent

Subjects
[SDV] Life Sciences [q-bio], [SDV]Life Sciences [q-bio], ComputingMilieux_MISCELLANEOUS
Abstract

International audience

Published
2019

12. Thrombocytopenia in the sepsis syndrome: role of hemophagocytosis and macrophage colony-stimulating factor

Author

Francois, B., Trimoreau, F., Vignon, P., Fixe, P., Praloran, V., and Gastinne, H.

Subjects
Thrombocytopenia -- Causes of, Macrophage colony stimulating factor -- Physiological aspects, Bacterial infections -- Complications, Health, Health care industry
Abstract

BACKGROUND: Thrombocytopenia is frequently encountered in critically ill patients with the sepsis syndrome, but its mechanisms frequently remain undetermined. Hemophagocytosis has been reported as a cause of thrombocytopenia in various diseases. This prospective study was designed to assess: (1) the incidence of hemophagocytosis in patients suffering from both the sepsis syndrome and unexplained thrombocytopenia, and (2) the circulating level of the macrophage-colony-stimulating factor (M-CSF) according to the presence or absence of hemophagocytosis. METHODS: Fifty consecutive patients diagnosed with both the sepsis syndrome and thrombocytopenia of undetermined origin were studied. Hemophagocytosis was diagnosed based on microscopical examination of sternal bone marrow aspiration by two independent observers. Serum M-CSF concentrations were measured in each patient and compared with levels of a normal population (n = 59). Causes and severity of sepsis syndromes as well as serum M-CSF levels were compared beween patients with and without hemophagocytosis. RESULTS: Hemophagocytosis was diagnosed in 32 patients (64%). Mean serum M-CSF levels were increased in patients when compared with normal subjects (539 [+ or -] 141 versus 208 [+ or -] 82 IU/mL: P < 0.001), and higher in patients with than without hemophagocytosis (580 [+ or -] 145 versus 457 [+ or -] 89 IU/mL: P = 0.01). Multiorgan dysfunction and infection were independent risk factors of hemophagocytosis (odds ratio = 31.3 and 6.8, 95% confidence interval (CI) = 5.4 to 177.6 and 1.0 to 47.4, P < 0.0001 and P = 0.03, respectively). CONCLUSIONS: Hemophagocytosis is a frequent cause of unexplained thrombocytopenia in patients with severe sepsis syndrome. Our results suggest that M-CSF is overproduced in the sepsis syndrome, particularly when hemophagocytosis is present. The role of M-CSF in the initiation and development of hemophagocytosis remains to be determined. Am J Med. 1997;103:114-120. [C] 1997 by Excerpta Medica, Inc.

Published
1997

16. FLT3-mediated p38-MAPK activation participates in the control of megakaryopoiesis in primary myelofibrosis

Author

Desterke, C., Bilhou-Nabera, C., Guerton, B., Martinaud, C., Tonetti, C., Clay, D., Guglielmelli, P., Vannucchi, A., Bordessoule, D., Hasselbalch, H., Dupriez, B., Benzoubir, N., Bourgeade, M.F., Pierre-Louis, O., Lazar, V., Vainchenker, W., Bennaceur-Griscelli, A., Gisslinger, H., Giraudier, S., Le Bousse-Kerdiles, M.C., Bourhis, J.H., de Botton, S., Briere, J., Demory, J.L., Fenaux, P., Kiladjian, J.J., Pasquet, J.M., Lippert, E., Praloran, V., Morel, P., Rey, J., Roy, L., Viallard, J.F., Barosi, G., Cervantes, F., Griesshammer, M., Kreipe, H., Kvasnicka, H.M., Kušec, Rajko, Marchetti, M., Merup, M., Pahl, H., Palmblad, J., Reilly, J.T., Skoda, R., and Thiele, J.

Subjects
MAPK/ERK pathway, Cancer Research, Stromal cell, MAP Kinase Signaling System, p38 mitogen-activated protein kinases, myelofibrosis, FLT3, MAPK, megakaryocytes, Antigens, CD34, Biology, p38 Mitogen-Activated Protein Kinases, Downregulation and upregulation, hemic and lymphatic diseases, Humans, Phosphorylation, Protein kinase A, FLT3, p38-MAPK, primary myelofibrosis, cancer, Megakaryopoiesis, Membrane Proteins, Hematopoietic Stem Cells, Enzyme Activation, Haematopoiesis, fms-Like Tyrosine Kinase 3, Oncology, Primary Myelofibrosis, Trk receptor, Leukocytes, Mononuclear, Cancer research, Mitogen-Activated Protein Kinases, Stromal Cells, Megakaryocytes
Abstract

Primary myelofibrosis (PMF) is characterized by increased number of hematopoietic progenitors and a dysmegakaryopoiesis which supports the stromal reaction defining this disease. We showed that increased ligand (FL) levels in plasma, hematopoietic progenitors, and stromal cells from PMF patients were associated with upregulation of the cognate Flt3 receptor on megakaryocytic (MK) cells. This connection prompted us to study a functional role for the FL/Flt3 couple in PMF dysmegakaryopoiesis, as a route to reveal insights into pathobiology and therapy in this disease. Analysis of PMF CD34+ and MK cell transcriptomes revealed deregulation of the mitogen-activated protein kinase (MAPK) pathway along with Flt3 expression. In PMF patients, a higher proportion of circulating Flt3+CD34+CD41+ cells exhibited an increased MAPK effector phosphorylation independently of Jak2V617F mutation. Activation of FL/Flt3 axis in PMF MK cell cultures, in response to FL, induced activation of the p38–MAPK cascade, which is known to be involved in inflammation, also increasing expression of its target genes (NFATC4, p53, AP-1, IL-8). Inhibiting Flt3 or MAPK or especially p38 by chemical, antibody, or silencing strategies restored megakaryopoiesis and reduced phosphorylation of Flt3 and p38 pathway effectors, confirming the involvement of Flt3 in PMF dysmegakaryopoiesis via p38 activation. In addition, in contrast to healthy donors, MK cells derived from PMF CD34+ cells exhibited an FL-induced migration that could be reversed by p38 inhibition. Taken together, our results implicate the FL/Flt3 ligand–receptor complex in PMF dysmegakaryopoiesis through persistent p38–MAPK activation, with implications for therapeutic prospects to correct altered megakaryopoiesis in an inflammatory context. Cancer Res; 71(8); 2901–15. ©2011 AACR.

Published
2011
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19. Serum levels of macrophage-colony stimulating factor (M-CSF): A marker of kidney allograft rejection.

Author

Praloran V., Mons S., Jose M., Dantal J., Lemauff B., Aldigier J.-C., Leroux-Robert C., Le Meur Y., Leprivey-Lorgeot V., Praloran V., Mons S., Jose M., Dantal J., Lemauff B., Aldigier J.-C., Leroux-Robert C., Le Meur Y., and Leprivey-Lorgeot V.

Abstract

Background. Macrophage-colony stimulating factor (M-CSF) is the principal factor for survival of monocytes and macrophages that play an important role in allograft rejection. We studied M-CSF serum levels during successful renal transplantation and acute graft rejection. Methods. A total of 114 kidney allograft recipients were assessed for M-CSF levels by enzyme-linked immunosorbent assay (ELISA). Results. M-CSF serum levels were elevated in pretransplant haemodialysis patients (611+/-355 IU/ml vs 168+/-61 in normal controls, P<0.01). Following successful renal transplantation, M-CSF decreased in the first month, stabilizing at 257+/-222IU/ml (not significantly different from normal controls) in 52 post-transplant stable patients. There was no correlation between M-CSF level and creatinine clearance. M-CSF levels increased significantly (2-5 times) during biopsy-proven acute rejection episodes in 20 of 25 patients. All rejection episodes were successfully treated and serum M-CSF decreased rapidly to pre-rejection levels in 17/20 patients. In contrast, in five patients with cyclosporin toxicity and four patients with other causes of allograft dysfunction, M-CSF serum levels did not change. Conclusions. M-CSF serum level might be a specific marker of acute rejection. The source of increased production during rejection warrants further investigation, with infiltrating T cells and resident kidney cells being likely candidates. © ERA-EDTA 2004; all rights reserved.

Published
2012

42. P3-11 Intérêt de la culture en gel de collagène pour la standardisation du comptage des CFU-GM et BFU-E des greffons de cellules souches priphériques (CSP): étude comparative multicentrique de kits commerciaux en collagène et méthylcellulose

Author

Dobo, I, primary, Mossuz, P, additional, Genevay, MC, additional, Allegraud, A, additional, Cousin, F, additional, Dautel, M, additional, Niaussat, AE, additional, Praloran, V, additional, Boccacio, C, additional, and Hermouet, S, additional

Published
1998
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