Search

Your search keyword '"Wielockx, Ben"' showing total 12 results
Start Over Author "Wielockx, Ben" Journal blood
12 results on '"Wielockx, Ben"'

4. HIF2α is a direct regulator of neutrophil motility

Author

Sormendi, Sundary, primary, Deygas, Mathieu, additional, Sinha, Anupam, additional, Bernard, Mathilde, additional, Krüger, Anja, additional, Kourtzelis, Ioannis, additional, Le Lay, Gregoire, additional, Sáez, Pablo J., additional, Gerlach, Michael, additional, Franke, Kristin, additional, Meneses, Ana, additional, Kräter, Martin, additional, Palladini, Alessandra, additional, Guck, Jochen, additional, Coskun, Ünal, additional, Chavakis, Triantafyllos, additional, Vargas, Pablo, additional, and Wielockx, Ben, additional

Published
2021
Full Text
View/download PDF

5. B Cell Specific Knockdown of the Erythropoietin (EPO) Receptor Attenuates EPO-Induced Bone Loss in Mice

Author

Kolomansky, Albert, primary, Deshet-Unger, Naamit, primary, Ben-Califa, Nathalie, primary, Awida, Zamzam, primary, Ibrahim, Maria, primary, Liron, Tamar, primary, Hiram-Bab, Sahar, primary, Oster, Howard S., primary, Mittelman, Moshe, primary, Rauner, Martina, primary, Wielockx, Ben, primary, Gabet, Yankel, primary, and Neumann, Drorit, primary

Published
2019
Full Text
View/download PDF

9. HIF-1α is a protective factor in conditional PHD2-deficient mice suffering from severe HIF-2α–induced excessive erythropoiesis

Author

Franke, Kristin, primary, Kalucka, Joanna, additional, Mamlouk, Soulafa, additional, Singh, Rashim Pal, additional, Muschter, Antje, additional, Weidemann, Alexander, additional, Iyengar, Vasuprada, additional, Jahn, Steffen, additional, Wieczorek, Kathrin, additional, Geiger, Kathrin, additional, Muders, Michael, additional, Sykes, Alex M., additional, Poitz, David M., additional, Ripich, Tatsiana, additional, Otto, Teresa, additional, Bergmann, Sybille, additional, Breier, Georg, additional, Baretton, Gustavo, additional, Fong, Guo-Hua, additional, Greaves, David R., additional, Bornstein, Stefan, additional, Chavakis, Triantafyllos, additional, Fandrey, Joachim, additional, Gassmann, Max, additional, and Wielockx, Ben, additional

Published
2013
Full Text
View/download PDF

10. Erythropoietin (EPO) Regulates Bone Mass ViaEPO Receptors on Myeloid and Lymphocytic Cells

Author

Hiram-Bab, Sahar, Kolomansky, Albert, Deshet-Unger, Naamit, Ben-Califa, Nathalie, Liron, Tamar, Rauner, Martina, Wielockx, Ben, Mittelman, Moshe, Oster, Howard S., Gabet, Yankel, and Neumann, Drorit

Abstract

Background and aims: Erythropoietin (EPO) is the key regulator of red blood cell production. In response to hypoxia, EPO levels can increase 1000-fold and remain high for weeks to promote hematopoiesis. Therapeutically, the introduction of EPO and erythropoietic stimulating agents into clinical practice has revolutionized the treatment of anemia despite certain concerns regarding the safety of the therapy. Recent studies demonstrate that EPO has activities in addition to hematopoiesis, and modulates bone remodeling by increasing bone resorption and decreasing bone formation, leading to trabecular bone loss. In vitro, EPO directly inhibits murine osteoblast differentiation and mineralization at doses relatively lower than those shown to stimulate osteoclastogenesis. The aim of this study was to investigate the dose-response relationship between EPO dose, hemoglobin (Hgb) levels, and the extent of bone loss, as well as to examine the role of the monocytic and B cell EPO receptor (EPOR) in bone metabolism.

Published
2018
Full Text
View/download PDF

11. Erythropoietin Stimulates Bone Resorption ViaDirect Activation of the Monocytic Lineage and ViaIncreased RANKL Production By B Cells and Osteoblasts

Author

Hiram-Bab, Sahar, Deshet, Naamit, Liron, Tamar, Mittelman, Moshe, Gassmann, Max, Rauner, Martina, Franke, Kristin, Wielockx, Ben, Gabet, Yankel, and Neumann, Drorit

Abstract

The negative effect of hypoxia on bone metabolism is well established but its mechanism of action is not fully understood. Hypoxia triggers the production of erythropoietin (EPO), a hormone most recognized for its hematopoietic function. An increasing number of roles unrelated to red blood cell production have been attributed to EPO, many of which are mediated by non-erythroid cells. In light of the controversy on the effect of increased serum levels of EPO on the skeleton, we investigated here the effect of the hormone on bone metabolism using EPO overexpressing (Tg6), and EPO-administered adult mice. In these models, the increase in EPO levels is similar to its physiologic increase at high altitude without the confounding direct effect of hypoxia on bone cells. Using microcomputed tomography, histology and serum markers we found that high EPO levels result in a severe trabecular bone loss (-32 to -61% decrease in bone density in Tg6 and EPO-injected animals, respectively; p<0.05 versustheir respective controls throughout), due to increased bone resorption (+28 to +18% in TRAP5b serum levels) and reduced bone formation rate (-19 to -74%). This bone loss consisted of reduced trabecular number, but not thickness, with no effect on the cortical bone compartment. A similar bone response was observed with high and low doses of EPO, with no difference between intermittent and continuous administration modes. Using flow cytometry analysis and specific cell surface markers, we found that EPO (both overexpression and injection) targets the monocytic lineage by increasing the number of CD115+CD265-monocytes/macrophages by 43 and 57% (p<0.05), CD115+CD265+pre-osteoclasts by 2 and 4-fold (p=0.02) and mature osteoclasts (TRAP positive) by 64 and 88% (p<0.05, Figure 1A) in bones, compared to WT and diluent controls, respectively.

Published
2014
Full Text
View/download PDF

12. HIF prolyl hydroxylase 2 (PHD2) is a critical regulator of hematopoietic stem cell maintenance during steady-state and stress.

Author

Pal Singh, Rashim, Franke, Kristin, Kalucka, Joanna, Mamlouk, Soulafa, Muschter, Antje, Gembarska, Agnieszka, Grinenko, Tatyana, Willam, Carsten, Naumann, Ronald, Anastassiadis, Konstantinos, Stewart, A. Francis, Bornstein, Stefan, Chavakis, Triantafyllos, Breier, Georg, Waskow, Claudia, and Wielockx, Ben

Subjects
*HYPOXEMIA, *HEMATOPOIETIC stem cells, *HYPOXIA-inducible factors, *OXYGEN detectors, *BONE marrow transplantation, *CHIMERISM
Abstract

Hypoxia is a prominent feature in the maintenance of hematopoietic stem cell (HSC) quiescence and multipotency. Hypoxia-inducible factor (HIF) prolyl hydroxylase domain proteins (PHDs) serve as oxygen sensors and may therefore regulate this system. Here, we describe a mouse line with conditional loss of HIF prolyl hydroxylase 2 (PHD2) in very early hematopoietic precursors that results in self-renewal of multipotent progenitors under steady-state conditions in a HlFlα- and SMAD7-dependent manner. Competitive bone marrow (BM) transplantations show decreased peripheral and central chimerism of PHD2-deficient cells but not of the most primitive progenitors. Conversely, in whole BM transfer, PHD2-deficient HSCs replenish the entire hematopoietic system and display an enhanced self-renewal capacity reliant on HIF1α. Taken together, our results demonstrate that loss of PHD2 controls the maintenance of the HSC compartment under physiological conditions and causes the outcompetition of PHD2-deficient hematopoietic cells by their wild-type counterparts during stress while promoting the self-renewal of very early hematopoletic progenitors. [ABSTRACT FROM AUTHOR]

Published
2013
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results