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469 results on '"Méndez Ferrer, Simón"'

123. Haematopoietic stem cells in perisinusoidal niches are protected from ageing

Author

Saçma, Mehmet, primary, Pospiech, Johannes, additional, Bogeska, Ruzhica, additional, de Back, Walter, additional, Mallm, Jan-Philipp, additional, Sakk, Vadim, additional, Soller, Karin, additional, Marka, Gina, additional, Vollmer, Angelika, additional, Karns, Rebekah, additional, Cabezas-Wallscheid, Nina, additional, Trumpp, Andreas, additional, Méndez-Ferrer, Simón, additional, Milsom, Michael D., additional, Mulaw, Medhanie A., additional, Geiger, Hartmut, additional, and Florian, Maria Carolina, additional

Published
2019
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125. Human and mouse leukocytes: different clockwork

Author

Méndez-Ferrer, Simón, Méndez-Ferrer, Simón [0000-0002-9805-9988], and Apollo - University of Cambridge Repository

Subjects
0301 basic medicine, Leukocyte migration, Immunology, Biology, Biochemistry, CXCR4, Mice, 03 medical and health sciences, Leukocyte Trafficking, Leukocytes, Animals, Humans, RNA, Messenger, Circadian rhythm, Receptor, chemistry.chemical_classification, Genetics, Reactive oxygen species, Cell Biology, Hematology, Circadian Rhythm, Cell biology, Crosstalk (biology), 030104 developmental biology, chemistry, Humanized mouse
Abstract

In this issue of Blood, Zhao et al use a humanized mouse model to investigate the mechanisms driving daily oscillations in circulating human and murine leukocytes.1 In the same mice, they find human and murine circulating leukocytes displaying inverted oscillations, reproducing the trafficking pattern previously observed in both species. A novel network regulating circadian leukocyte trafficking is proposed. It involves interspecies differences of stress-kinase regulation of reactive oxygen species (ROS), hypoxia-inducible factor 1a (HIF-1a) and clock gene–dependent regulation of the CXCL12 receptor CXCR4. This study underscores the crosstalk of the genetic clock with metabolism and ROS in the regulation of leukocyte migration and reveals new mechanistic players.

Published
2017
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128. Hematopoietic Stem Cells in Perisinusoidal Niches are Protected From Aging

Author

Sacma, Mehmet, primary, Pospiech, Johannes, additional, Bogeska, Ruzhica, additional, de Back, Walter, additional, Karns, Rebekah, additional, Sakk, Vadim, additional, Soller, Karin, additional, Marka, Gina, additional, Vollmer, Angelika, additional, Méndez-Ferrer, Simón, additional, Cabezas-Wallscheid, Nina, additional, Trumpp, Andreas, additional, Milsom, Michael D., additional, Geiger, Hartmut, additional, and Florian, Maria Carolina, additional

Published
2018
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130. Network anatomy and in vivo physiology of mesenchymal stem and stromal cells

Author

Méndez-Ferrer Simón and Lorena Arranz

Subjects
Immunology, Mesenchymal stem cell, Hematopoietic stem cell, Clinical uses of mesenchymal stem cells, Stem cell factor, Biology, medicine.anatomical_structure, Cancer stem cell, medicine, Immunology and Allergy, Stem cell, Neuroscience, Stem cell transplantation for articular cartilage repair, Adult stem cell
Abstract

Over the last few years, the mesenchymal stromal compartment of the bone marrow has regained interest. The main reason for this resurgence is the recognition of their immunomodulatory properties and their prominent role in the maintenance and regulation of hematopoiesis. This has simultaneously prompted preclinical and clinical studies trying to take advantage of these properties and, at the same time, basic studies that have tried to dissect the bone marrow stromal compartment and the specific functions that different stromal cells have in the regulation of hematopoiesis and immunity. In this minireview we will summarize our contributions to the functions of mesenchymal stem cells in regulating hematopoietic stem cells. By putting them in a broader context, we will discuss the emerging role of mesenchymal stem cells as key integrators of neuro-endocrine signals, able to couple whole-organism demands to fine-tuned responses in remote stem cell niches. Rec.12/4/2012, Acc.12/10/2012, pp38-47

Published
2013
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133. Nestin(+) cells direct inflammatory cell migration in atherosclerosis

Author

Toro, Raquel del, Chèvre, Raphael, Rodríguez, Cristina, Ordóñez Fernández, Antonio, Martínez-González, José, Andrés, Vicente, Méndez-Ferrer, Simón, Fundación ProCNIC, Ministerio de Economía y Competitividad (España), Wellcome Trust, MRC Cambridge Stem Cell Institute, Comunidad de Madrid (España), Unión Europea. Comisión Europea, Howard Hughes Medical Institute, NHS - Blood and Transplant (Reino Unido), Instituto de Biomedicina de Sevilla, Fundación Pro CNIC, Red de Terapia Celular (España), European Commission, Comunidad de Madrid, British Blood Transfusion Society, European Research Council, Universidad de Sevilla. Departamento de Fisiología Médica y Biofísica, Universidad de Sevilla. Departamento de Cirugía, and Apollo - University of Cambridge Repository

Subjects
Neutrophils, Science, SMOOTH-MUSCLE-CELLS, education, macromolecular substances, Nestinþ cells, MYELOID CALCIFYING CELLS, Diet, High-Fat, Article, Monocytes, Mesoderm, Nestin, Mice, Apolipoproteins E, Cell Movement, Animals, Aorta, Chemokine CCL2, Inflammation, Mice, Knockout, MESENCHYMAL STEM, Apolipoprotein E (ApoE), Endothelial Cells, Nestin+ Cells, Atherosclerosis, Inflammatory cell migration, ENDOTHELIAL-CELLS, Plaque, Atherosclerotic, Mice, Inbred C57BL, nervous system, PROGENITOR CELLS, HEMATOPOIETIC STEM, NEOINTIMA FORMATION, MONOCYTE RECRUITMENT, embryonic structures, VASA-VASORUM, STEM-CELLS
Abstract

Atherosclerosis is a leading death cause. Endothelial and smooth muscle cells participate in atherogenesis, but it is unclear whether other mesenchymal cells contribute to this process. Bone marrow (BM) nestin+ cells cooperate with endothelial cells in directing monocyte egress to bloodstream in response to infections. However, it remains unknown whether nestin+ cells regulate inflammatory cells in chronic inflammatory diseases, such as atherosclerosis. Here, we show that nestin+ cells direct inflammatory cell migration during chronic inflammation. In Apolipoprotein E (ApoE) knockout mice fed with high-fat diet, BM nestin+ cells regulate the egress of inflammatory monocytes and neutrophils. In the aorta, nestin+ stromal cells increase ∼30 times and contribute to the atheroma plaque. Mcp1 deletion in nestin+ cells—but not in endothelial cells only— increases circulating inflammatory cells, but decreases their aortic infiltration, delaying atheroma plaque formation and aortic valve calcification. Therefore, nestin expression marks cells that regulate inflammatory cell migration during atherosclerosis., Bone marrow cells producing the intermediate filament nestin guide monocyte egress to the bloodstream in response to infection. Here, the authors show that nestin-producing stromal cells direct inflammatory cell migration in atherosclerosis, and that stromal Mcp1 is crucial in this process.

Published
2016

137. Nestin(+) cells direct inflammatory cell migration in atherosclerosis

Author

Universidad de Sevilla. Departamento de Fisiología Médica y Biofísica, Universidad de Sevilla. Departamento de Cirugía, Toro, Raquel del, Chèvre, Raphael, Rodríguez, Cristina, Ordoñez, Antonio, Martínez González, José, Andrés, Vicente, Méndez Ferrer, Simón, Universidad de Sevilla. Departamento de Fisiología Médica y Biofísica, Universidad de Sevilla. Departamento de Cirugía, Toro, Raquel del, Chèvre, Raphael, Rodríguez, Cristina, Ordoñez, Antonio, Martínez González, José, Andrés, Vicente, and Méndez Ferrer, Simón

Abstract

Atherosclerosis is a leading death cause. Endothelial and smooth muscle cells participate in atherogenesis, but it is unclear whether other mesenchymal cells contribute to this process. Bone marrow (BM) nestinþ cells cooperate with endothelial cells in directing monocyte egress to bloodstream in response to infections. However, it remains unknown whether nestinþ cells regulate inflammatory cells in chronic inflammatory diseases, such as atherosclerosis. Here, we show that nestinþ cells direct inflammatory cell migration during chronic inflammation. In Apolipoprotein E (ApoE) knockout mice fed with high-fat diet, BM nestinþ cells regulate the egress of inflammatory monocytes and neutrophils. In the aorta, nestinþ stromal cells increase B30 times and contribute to the atheroma plaque. Mcp1 deletion in nestinþ cells—but not in endothelial cells only— increases circulating inflammatory cells, but decreases their aortic infiltration, delaying atheroma plaque formation and aortic valve calcification. Therefore, nestin expression marks cells that regulate inflammatory cell migration during atherosclerosis.

Published
2016

138. Nestinþ cells direct inflammatory cell migration in atherosclerosis

Author

Instituto de Biomedicina de Sevilla, Toro, Raquel del, Chevre, Raphael, Rodríguez, Cristina, Ordoñez, Antonio, Martinez Gonzalez, José, Andrés, Vicente, Méndez Ferrer, Simón, Instituto de Biomedicina de Sevilla, Toro, Raquel del, Chevre, Raphael, Rodríguez, Cristina, Ordoñez, Antonio, Martinez Gonzalez, José, Andrés, Vicente, and Méndez Ferrer, Simón

Abstract

Atherosclerosis is a leading death cause. Endothelial and smooth muscle cells participate in atherogenesis, but it is unclear whether other mesenchymal cells contribute to this process. Bone marrow (BM) nestinþ cells cooperate with endothelial cells in directing monocyte egress to bloodstream in response to infections. However, it remains unknown whether nestinþ cells regulate inflammatory cells in chronic inflammatory diseases, such as atherosclerosis. Here, we show that nestinþ cells direct inflammatory cell migration during chronic inflammation. In Apolipoprotein E (ApoE) knockout mice fed with high-fat diet, BM nestinþ cells regulate the egress of inflammatory monocytes and neutrophils. In the aorta, nestinþ stromal cells increase B30 times and contribute to the atheroma plaque. Mcp1 deletion in nestinþ cells—but not in endothelial cells only— increases circulating inflammatory cells, but decreases their aortic infiltration, delaying atheroma plaque formation and aortic valve calcification. Therefore, nestin expression marks cells that regulate inflammatory cell migration during atherosclerosis.

Published
2016

139. The European Hematology Association Roadmap for European Hematology Research: a consensus document.

Author

EHA Roadmap for European Hematology, Research, Engert, A., Balduini, C., Brand, A., Coiffier, B., Cordonnier, C., Döhner, H., de Wit TD., Eichinger, S., Fibbe, W., Green, T., de Haas, F., Iolascon, A., Jaffredo, T., Rodeghiero, F., Salles, G., Schuringa, JJ., André, M., Andre-Schmutz, I., Bacigalupo, A., Bochud, PY., Boer, Md., Bonini, C., Camaschella, C., Cant, A., Cappellini, MD., Cazzola, M., Celso, CL., Dimopoulos, M., Douay, L., Dzierzak, E., Einsele, H., Ferreri, A., De Franceschi, L., Gaulard, P., Gottgens, B., Greinacher, A., Gresele, P., Gribben, J., de Haan, G., Hansen, JB., Hochhaus, A., Kadir, R., Kaveri, S., Kouskoff, V., Kühne, T., Kyrle, P., Ljungman, P., Maschmeyer, G., Méndez-Ferrer£££Simón£££ S., Milsom, M., Mummery, C., Ossenkoppele, G., Pecci, A., Peyvandi, F., Philipsen, S., Reitsma, P., Ribera, JM., Risitano, A., Rivella, S., Ruf, W., Schroeder, T., Scully, M., Socie, G., Staal, F., Stanworth, S., Stauder, R., Stilgenbauer, S., Tamary, H., Theilgaard-Mönch, K., Thein, SL., Tilly, H., Trneny, M., Vainchenker, W., Vannucchi, AM., Viscoli, C., Vrielink, H., Zaaijer, H., Zanella, A., Zolla, L., Zwaginga, JJ., Martinez, PA., van den Akker, E., Allard, S., Anagnou, N., Andolfo, I., Andrau, JC., Angelucci, E., Anstee, D., Aurer, I., Avet-Loiseau, H., Aydinok, Y., Bakchoul, T., Balduini, A., Barcellini, W., Baruch, D., Baruchel, A., Bayry, J., Bento, C., van den Berg, A., Bernardi, R., Bianchi, P., Bigas, A., Biondi, A., Bohonek, M., Bonnet, D., Borchmann, P., Borregaard, N., Brækkan, S., van den Brink, M., Brodin, E., Bullinger, L., Buske, C., Butzeck, B., Cammenga, J., Campo, E., Carbone, A., Cervantes, F., Cesaro, S., Charbord, P., Claas, F., Cohen, H., Conard, J., Coppo, P., Corrons, JL., Costa, Ld., Davi, F., Delwel, R., Dianzani, I., Domanović, D., Donnelly, P., Drnov?ek£££Tadeja Dovč£££ TD., Dreyling, M., Du, MQ., Dufour, C., Durand, C., Efremov, D., Eleftheriou, A., Elion, J., Emonts, M., Engelhardt, M., Ezine, S., Falkenburg, F., Favier, R., Federico, M., Fenaux, P., Fitzgibbon, J., Flygare, J., Foà, R., Forrester, L., Galacteros, F., Garagiola, I., Gardiner, C., Garraud, O., van Geet, C., Geiger, H., Geissler, J., Germing, U., Ghevaert, C., Girelli, D., Godeau, B., Gökbuget, N., Goldschmidt, H., Goodeve, A., Graf, T., Graziadei, G., Griesshammer, M., Gruel, Y., Guilhot, F., von Gunten, S., Gyssens, I., Halter, J., Harrison, C., Harteveld, C., Hellström-Lindberg, E., Hermine, O., Higgs, D., Hillmen, P., Hirsch, H., Hoskin, P., Huls, G., Inati, A., Johnson, P., Kattamis, A., Kiefel, V., Kleanthous, M., Klump, H., Krause, D., Hovinga, JK., Lacaud, G., Lacroix-Desmazes, S., Landman-Parker, J., LeGouill, S., Lenz, G., von Lilienfeld-Toal, M., von Lindern, M., Lopez-Guillermo, A., Lopriore, E., Lozano, M., MacIntyre, E., Makris, M., Mannhalter, C., Martens, J., Mathas, S., Matzdorff, A., Medvinsky, A., Menendez, P., Migliaccio, AR., Miharada, K., Mikulska, M., Minard, V., Montalbán, C., de Montalembert, M., Montserrat, E., Morange, PE., Mountford, J., Muckenthaler, M., Müller-Tidow, C., Mumford, A., Nadel, B., Navarro, JT., Nemer, We., Noizat-Pirenne, F., O'Mahony, B., Oldenburg, J., Olsson, M., Oostendorp, R., Palumbo, A., Passamonti, F., Patient, R., Peffault, R., Pflumio, F., Pierelli, L., Piga, A., Pollard, D., Raaijmakers, M., Radford, J., Rambach, R., Rao, AK., Raslova, H., Rebulla, P., Rees, D., Ribrag, V., Rijneveld, A., Rinalducci, S., Robak, T., Roberts, I., Rodrigues, C., Rosendaal, F., Rosenwald, A., Rule, S., Russo, R., Saglio, G., Sanchez, M., Scharf, RE., Schlenke, P., Semple, J., Sierra, J., So-Osman, C., Soria, JM., Stamatopoulos, K., Stegmayr, B., Stunnenberg, H., Swinkels, D., Barata£££João Pedro Taborda£££ JP., Taghon, T., Taher, A., Terpos, E., Thachil, J., Tissot, JD., Touw, I., Toye, A., Trappe, R., Traverse-Glehen, A., Unal, S., Vaulont, S., Viprakasit, V., Vitolo, U., van Wijk, R., Wójtowicz, A., Zeerleder, S., Zieger, B., de Wit, T.D., Schuringa, J.J., EHA Roadmap for European Hematology, Research, Engert, A., Balduini, C., Brand, A., Coiffier, B., Cordonnier, C., Döhner, H., de Wit TD., Eichinger, S., Fibbe, W., Green, T., de Haas, F., Iolascon, A., Jaffredo, T., Rodeghiero, F., Salles, G., Schuringa, JJ., André, M., Andre-Schmutz, I., Bacigalupo, A., Bochud, PY., Boer, Md., Bonini, C., Camaschella, C., Cant, A., Cappellini, MD., Cazzola, M., Celso, CL., Dimopoulos, M., Douay, L., Dzierzak, E., Einsele, H., Ferreri, A., De Franceschi, L., Gaulard, P., Gottgens, B., Greinacher, A., Gresele, P., Gribben, J., de Haan, G., Hansen, JB., Hochhaus, A., Kadir, R., Kaveri, S., Kouskoff, V., Kühne, T., Kyrle, P., Ljungman, P., Maschmeyer, G., Méndez-Ferrer£££Simón£££ S., Milsom, M., Mummery, C., Ossenkoppele, G., Pecci, A., Peyvandi, F., Philipsen, S., Reitsma, P., Ribera, JM., Risitano, A., Rivella, S., Ruf, W., Schroeder, T., Scully, M., Socie, G., Staal, F., Stanworth, S., Stauder, R., Stilgenbauer, S., Tamary, H., Theilgaard-Mönch, K., Thein, SL., Tilly, H., Trneny, M., Vainchenker, W., Vannucchi, AM., Viscoli, C., Vrielink, H., Zaaijer, H., Zanella, A., Zolla, L., Zwaginga, JJ., Martinez, PA., van den Akker, E., Allard, S., Anagnou, N., Andolfo, I., Andrau, JC., Angelucci, E., Anstee, D., Aurer, I., Avet-Loiseau, H., Aydinok, Y., Bakchoul, T., Balduini, A., Barcellini, W., Baruch, D., Baruchel, A., Bayry, J., Bento, C., van den Berg, A., Bernardi, R., Bianchi, P., Bigas, A., Biondi, A., Bohonek, M., Bonnet, D., Borchmann, P., Borregaard, N., Brækkan, S., van den Brink, M., Brodin, E., Bullinger, L., Buske, C., Butzeck, B., Cammenga, J., Campo, E., Carbone, A., Cervantes, F., Cesaro, S., Charbord, P., Claas, F., Cohen, H., Conard, J., Coppo, P., Corrons, JL., Costa, Ld., Davi, F., Delwel, R., Dianzani, I., Domanović, D., Donnelly, P., Drnov?ek£££Tadeja Dovč£££ TD., Dreyling, M., Du, MQ., Dufour, C., Durand, C., Efremov, D., Eleftheriou, A., Elion, J., Emonts, M., Engelhardt, M., Ezine, S., Falkenburg, F., Favier, R., Federico, M., Fenaux, P., Fitzgibbon, J., Flygare, J., Foà, R., Forrester, L., Galacteros, F., Garagiola, I., Gardiner, C., Garraud, O., van Geet, C., Geiger, H., Geissler, J., Germing, U., Ghevaert, C., Girelli, D., Godeau, B., Gökbuget, N., Goldschmidt, H., Goodeve, A., Graf, T., Graziadei, G., Griesshammer, M., Gruel, Y., Guilhot, F., von Gunten, S., Gyssens, I., Halter, J., Harrison, C., Harteveld, C., Hellström-Lindberg, E., Hermine, O., Higgs, D., Hillmen, P., Hirsch, H., Hoskin, P., Huls, G., Inati, A., Johnson, P., Kattamis, A., Kiefel, V., Kleanthous, M., Klump, H., Krause, D., Hovinga, JK., Lacaud, G., Lacroix-Desmazes, S., Landman-Parker, J., LeGouill, S., Lenz, G., von Lilienfeld-Toal, M., von Lindern, M., Lopez-Guillermo, A., Lopriore, E., Lozano, M., MacIntyre, E., Makris, M., Mannhalter, C., Martens, J., Mathas, S., Matzdorff, A., Medvinsky, A., Menendez, P., Migliaccio, AR., Miharada, K., Mikulska, M., Minard, V., Montalbán, C., de Montalembert, M., Montserrat, E., Morange, PE., Mountford, J., Muckenthaler, M., Müller-Tidow, C., Mumford, A., Nadel, B., Navarro, JT., Nemer, We., Noizat-Pirenne, F., O'Mahony, B., Oldenburg, J., Olsson, M., Oostendorp, R., Palumbo, A., Passamonti, F., Patient, R., Peffault, R., Pflumio, F., Pierelli, L., Piga, A., Pollard, D., Raaijmakers, M., Radford, J., Rambach, R., Rao, AK., Raslova, H., Rebulla, P., Rees, D., Ribrag, V., Rijneveld, A., Rinalducci, S., Robak, T., Roberts, I., Rodrigues, C., Rosendaal, F., Rosenwald, A., Rule, S., Russo, R., Saglio, G., Sanchez, M., Scharf, RE., Schlenke, P., Semple, J., Sierra, J., So-Osman, C., Soria, JM., Stamatopoulos, K., Stegmayr, B., Stunnenberg, H., Swinkels, D., Barata£££João Pedro Taborda£££ JP., Taghon, T., Taher, A., Terpos, E., Thachil, J., Tissot, JD., Touw, I., Toye, A., Trappe, R., Traverse-Glehen, A., Unal, S., Vaulont, S., Viprakasit, V., Vitolo, U., van Wijk, R., Wójtowicz, A., Zeerleder, S., Zieger, B., de Wit, T.D., and Schuringa, J.J.

Abstract

The European Hematology Association (EHA) Roadmap for European Hematology Research highlights major achievements in diagnosis and treatment of blood disorders and identifies the greatest unmet clinical and scientific needs in those areas to enable better funded, more focused European hematology research. Initiated by the EHA, around 300 experts contributed to the consensus document, which will help European policy makers, research funders, research organizations, researchers, and patient groups make better informed decisions on hematology research. It also aims to raise public awareness of the burden of blood disorders on European society, which purely in economic terms is estimated at euro23 billion per year, a level of cost that is not matched in current European hematology research funding. In recent decades, hematology research has improved our fundamental understanding of the biology of blood disorders, and has improved diagnostics and treatments, sometimes in revolutionary ways. This progress highlights the potential of focused basic research programs such as this EHA Roadmap.The EHA Roadmap identifies nine 'sections' in hematology: normal hematopoiesis, malignant lymphoid and myeloid diseases, anemias and related diseases, platelet disorders, blood coagulation and hemostatic disorders, transfusion medicine, infections in hematology, and hematopoietic stem cell transplantation. These sections span 60 smaller groups of diseases or disorders.The EHA Roadmap identifies priorities and needs across the field of hematology, including those to develop targeted therapies based on genomic profiling and chemical biology, to eradicate minimal residual malignant disease, and to develop cellular immunotherapies, combination treatments, gene therapies, hematopoietic stem cell treatments, and treatments that are better tolerated by elderly patients.

Published
2016

140. Nestin+ cells direct inflammatory cell migration in atherosclerosis

Author

Fundación Pro CNIC, Wellcome Trust, Ministerio de Economía y Competitividad (España), MRC Cambridge Stem Cell Institute, Red de Terapia Celular (España), European Commission, Comunidad de Madrid, British Blood Transfusion Society, European Research Council, Howard Hughes Medical Institute, Toro, Raquel del, Chèvre, Raphael, Rodríguez-Sinovas, Cristina, Ordóñez Fernández, Antonio, Martínez-González, José, Andrés, Vicente, Méndez-Ferrer, Simón, Fundación Pro CNIC, Wellcome Trust, Ministerio de Economía y Competitividad (España), MRC Cambridge Stem Cell Institute, Red de Terapia Celular (España), European Commission, Comunidad de Madrid, British Blood Transfusion Society, European Research Council, Howard Hughes Medical Institute, Toro, Raquel del, Chèvre, Raphael, Rodríguez-Sinovas, Cristina, Ordóñez Fernández, Antonio, Martínez-González, José, Andrés, Vicente, and Méndez-Ferrer, Simón

Abstract

Atherosclerosis is a leading death cause. Endothelial and smooth muscle cells participate in atherogenesis, but it is unclear whether other mesenchymal cells contribute to this process. Bone marrow (BM) nestin+ cells cooperate with endothelial cells in directing monocyte egress to bloodstream in response to infections. However, it remains unknown whether nestin+ cells regulate inflammatory cells in chronic inflammatory diseases, such as atherosclerosis. Here, we show that nestin+ cells direct inflammatory cell migration during chronic inflammation. In Apolipoprotein E (ApoE) knockout mice fed with high-fat diet, BM nestin+ cells regulate the egress of inflammatory monocytes and neutrophils. In the aorta, nestin+ stromal cells increase ∼30 times and contribute to the atheroma plaque. Mcp1 deletion in nestin+ cells—but not in endothelial cells only— increases circulating inflammatory cells, but decreases their aortic infiltration, delaying atheroma plaque formation and aortic valve calcification. Therefore, nestin expression marks cells that regulate inflammatory cell migration during atherosclerosis.

Published
2016

141. Role of VHL, HIF1A and SDH on the expression of miR-210: Implications for tumoral pseudo-hypoxic fate

Author

Merlo, Anna, primary, Bernardo-Castiñeira, Cristóbal, additional, Sáenz-de-Santa-María, Inés, additional, Pitiot, Ana S, additional, Balbín, Milagros, additional, Astudillo, Aurora, additional, Valdés, Nuria, additional, Scola, Bartolomé, additional, Del Toro, Raquel, additional, Méndez-Ferrer, Simón, additional, I Piruat, José, additional, Suarez, Carlos, additional, and Chiara, María-Dolores, additional

Published
2016
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146. Aging of Bone Marrow Microenvironment Promotes Myeloid Bias of Hematopoietic Progenitors and Is a Target in Age-Related Myeloproliferative Neoplasms

Author

Ho, Ya-Hsuan, del Toro, Raquel, Rivera-Torres, José, Rak, Justyna, Korn, Claudia, García-García, Andrés, Kubovcakova, Lucia, Macías, David, Arranz, Lorena, González-Gómez, Cristina, Wittner, Monika, Nienhold, Ronny, Waller, Amie K, Foster, Holly R, Lopez-Otin, Carlos, Johnson, Randall S, Nerlov, Claus, Vainchenker, William, Ghevaert, Cedric, Louache, Fawzia, Skoda, Radek C., Andrés, Vicente, and Mendez-Ferrer, Simon

Published
2018
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148. Niche Heterogeneity Impacts Evolution of Myeloproliferative Neoplasms Driven By the Same Oncogenic Pathway

Author

Korn, Claudia, Rak, Justyna, García-García, Andrés, Fielding, Claire, Khorshed, Reema, González-Antón, Sara, Li, Juan, Norfo, Ruggiero, Baxter, E Joanna, McKerrell, Thomas, Roberts, Thomas, Eldaly, Hesham, Godfrey, Anna L, Castillo-Venzor, Aracely, Kusumbe, Anjali, Mead, Adam J., Green, Anthony R, Kent, David, Lo Celso, Cristina, and Mendez-Ferrer, Simon

Published
2018
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