Mirta Schattner

Summary

Affiliation: Academia Nacional de Medicina
Country: Argentina

Publications

  1. pmc Junín virus infection of human hematopoietic progenitors impairs in vitro proplatelet formation and platelet release via a bystander effect involving type I IFN signaling
    Roberto G Pozner
    Department of Thrombosis and Hemostasis, Hematological Research Institute Mariano R Castex, National Academy of Medicine, CONICET, Buenos Aires, Argentina
    PLoS Pathog 6:e1000847. 2010
  2. ncbi request reprint Functional responses and molecular mechanisms involved in histone-mediated platelet activation
    A Carestia
    Mirta Schattner, Instituto de Medicina Experimental, CONICET ANM, Pacheco de Melo 3081, Buenos Aires 1425, Argentina, Tel 54 11 4805 5759 ext 301, Fax 54 11 4805 0712, E mail
    Thromb Haemost 110:1035-45. 2013
  3. pmc Pathogenic mechanisms involved in the hematological alterations of arenavirus-induced hemorrhagic fevers
    Mirta Schattner
    Laboratory of Experimental Thrombosis, Institute of Experimental Medicine, CONICET, National Academy of Medicine Pacheco de Melo 3081 1425, Buenos Aires, Argentina
    Viruses 5:340-51. 2013
  4. doi request reprint Regulation of neutrophil extracellular trap formation by anti-inflammatory drugs
    Maria Jose Lapponi
    Laboratory of Experimental Thrombosis, Institute of Experimental Medicine, CONICET National Academy of Medicine, Buenos Aires, Argentina
    J Pharmacol Exp Ther 345:430-7. 2013
  5. ncbi request reprint Activation of cyclic AMP pathway prevents CD34(+) cell apoptosis
    Soledad Negrotto
    Hematological Research Institute, National Academy of Medicine, National Research Council CONICET, Buenos Aires, Argentina
    Exp Hematol 34:1420-8. 2006
  6. doi request reprint Astrocyte response to Junín virus infection
    Roberto G Pozner
    Thrombosis 1 Laboratory, Haematological Research Institute, National Academy of Medicine, Pacheco de Melo 3081, 1425 Buenos Aires, Argentina
    Neurosci Lett 445:31-5. 2008
  7. ncbi request reprint The immunoregulatory glycan-binding protein galectin-1 triggers human platelet activation
    Natalia Pacienza
    Hematological Research Institute, National Academy of Medicine, Buenos Aires, Argentina
    FASEB J 22:1113-23. 2008
  8. ncbi request reprint The low viability of human CD34+ cells under acidic conditions is improved by exposure to thrombopoietin, stem cell factor, interleukin-3, or increased cyclic adenosine monophosphate levels
    Lina Paola D'Atri
    Thrombosis I Laboratory, Hematological Research Institute Mariano R Castex, National Academy of Medicine, CONICET, Buenos Aires, Argentina
    Transfusion 51:1784-95. 2011
  9. doi request reprint Acidosis downregulates platelet haemostatic functions and promotes neutrophil proinflammatory responses mediated by platelets
    Julia Etulain
    Thrombosis I Laboratory, National Academy of Medicine, CONICET, Buenos Aires, Argentina
    Thromb Haemost 107:99-110. 2012
  10. doi request reprint Paracrine regulation of megakaryo/thrombopoiesis by macrophages
    Lina Paola D'Atri
    Thrombosis I Laboratory, Hematological Research Institute Mariano R Castex, National Academy of Medicine, CONICET, Buenos Aires, Argentina
    Exp Hematol 39:763-72. 2011

Collaborators

  • Ricardo M Gomez
  • Gabriel A Rabinovich
  • Maria Virginia Tribulatti
  • Ana Marisa Chudzinski-Tavassi
  • C Fondevila
  • Marina V Atzingen
  • Soledad Negrotto
  • Julia Etulain
  • Roberto G Pozner
  • Lina Paola D'Atri
  • Maria Albertina Romaniuk
  • Roberto Gabriel Pozner
  • Maria Jose Lapponi
  • Oscar Campetella
  • Leonardo Rivadeneyra
  • Agostina Carestia
  • Oscar Torres
  • Natalia Pacienza
  • Gabriela Pretre
  • A Carestia
  • Maria A Romaniuk
  • Verónica Inés Landoni
  • Diego O Croci
  • Carolina Jaquenod de Giusti
  • Agustín E Ure
  • Lina P D'Atri
  • Victor Romanowski
  • Elisa Malaver
  • Maria Angela Lazzari
  • Diego Omar Croci
  • Julieta Carabelli
  • M A Romaniuk
  • L Rivadeneyra
  • S Negrotto
  • Ana L T O Nascimento
  • Francoise Poirier
  • Giannoula Lakka Klement
  • María J Lapponi
  • Karen Amelia Nahmod
  • Martín Isturiz
  • Felisa Concepcion Molinas
  • Valentina Cattaneo
  • Joseph E Italiano
  • German A Bianco
  • Soledad Collado
  • Marina E Biedma
  • Mónica Lidia Kotler
  • Maria I Berria

Detail Information

Publications22

  1. pmc Junín virus infection of human hematopoietic progenitors impairs in vitro proplatelet formation and platelet release via a bystander effect involving type I IFN signaling
    Roberto G Pozner
    Department of Thrombosis and Hemostasis, Hematological Research Institute Mariano R Castex, National Academy of Medicine, CONICET, Buenos Aires, Argentina
    PLoS Pathog 6:e1000847. 2010
    ..Our study introduces a potential mechanism for thrombocytopenia in VHF and other diseases associated with increased bone marrow type I IFN levels...
  2. ncbi request reprint Functional responses and molecular mechanisms involved in histone-mediated platelet activation
    A Carestia
    Mirta Schattner, Instituto de Medicina Experimental, CONICET ANM, Pacheco de Melo 3081, Buenos Aires 1425, Argentina, Tel 54 11 4805 5759 ext 301, Fax 54 11 4805 0712, E mail
    Thromb Haemost 110:1035-45. 2013
    ..Our data identify histones as important triggers of haemostatic and proinflammatory platelet responses, and only haemostatic responses are partially inhibited by anti-inflammatory drugs. ..
  3. pmc Pathogenic mechanisms involved in the hematological alterations of arenavirus-induced hemorrhagic fevers
    Mirta Schattner
    Laboratory of Experimental Thrombosis, Institute of Experimental Medicine, CONICET, National Academy of Medicine Pacheco de Melo 3081 1425, Buenos Aires, Argentina
    Viruses 5:340-51. 2013
    ..In this article, we present the current knowledge about the hematological alterations present in VHF induced by arenaviruses, including new aspects on the underlying pathogenic mechanisms...
  4. doi request reprint Regulation of neutrophil extracellular trap formation by anti-inflammatory drugs
    Maria Jose Lapponi
    Laboratory of Experimental Thrombosis, Institute of Experimental Medicine, CONICET National Academy of Medicine, Buenos Aires, Argentina
    J Pharmacol Exp Ther 345:430-7. 2013
    ..Our results show that NETs have an important role in the local control of infection and that ASA and NF-κB blockade could be useful therapies to avoid undesired effect of persistent neutrophil activation...
  5. ncbi request reprint Activation of cyclic AMP pathway prevents CD34(+) cell apoptosis
    Soledad Negrotto
    Hematological Research Institute, National Academy of Medicine, National Research Council CONICET, Buenos Aires, Argentina
    Exp Hematol 34:1420-8. 2006
    ..We have recently demonstrated that in CD34(+)-derived megakaryocytes, cAMP-related agents prevent apoptosis. In this study we addressed the question of whether cAMP also regulates survival of their precursors, CD34(+) cells...
  6. doi request reprint Astrocyte response to Junín virus infection
    Roberto G Pozner
    Thrombosis 1 Laboratory, Haematological Research Institute, National Academy of Medicine, Pacheco de Melo 3081, 1425 Buenos Aires, Argentina
    Neurosci Lett 445:31-5. 2008
    ....
  7. ncbi request reprint The immunoregulatory glycan-binding protein galectin-1 triggers human platelet activation
    Natalia Pacienza
    Hematological Research Institute, National Academy of Medicine, Buenos Aires, Argentina
    FASEB J 22:1113-23. 2008
    ..Our study reveals a novel unrecognized role for galectin-1 in the control of platelet physiology with potential implications in thrombosis, inflammation, and metastasis...
  8. ncbi request reprint The low viability of human CD34+ cells under acidic conditions is improved by exposure to thrombopoietin, stem cell factor, interleukin-3, or increased cyclic adenosine monophosphate levels
    Lina Paola D'Atri
    Thrombosis I Laboratory, Hematological Research Institute Mariano R Castex, National Academy of Medicine, CONICET, Buenos Aires, Argentina
    Transfusion 51:1784-95. 2011
    ..Because extracellular acidosis is a common feature of injured tissues or the tumor microenvironment and is a critical regulator of cell survival and activation, we evaluated the impact of acidosis on CD34+ cell biology...
  9. doi request reprint Acidosis downregulates platelet haemostatic functions and promotes neutrophil proinflammatory responses mediated by platelets
    Julia Etulain
    Thrombosis I Laboratory, National Academy of Medicine, CONICET, Buenos Aires, Argentina
    Thromb Haemost 107:99-110. 2012
    ..In conclusion, our results indicate that extracellular acidosis downregulates most of the haemostatic platelet functions, and promotes those involved in amplifying the neutrophil-mediated inflammatory response...
  10. doi request reprint Paracrine regulation of megakaryo/thrombopoiesis by macrophages
    Lina Paola D'Atri
    Thrombosis I Laboratory, Hematological Research Institute Mariano R Castex, National Academy of Medicine, CONICET, Buenos Aires, Argentina
    Exp Hematol 39:763-72. 2011
    ....
  11. doi request reprint Binding of galectin-1 to αIIbβ₃ integrin triggers "outside-in" signals, stimulates platelet activation, and controls primary hemostasis
    Maria A Romaniuk
    Laboratory of Experimental Thrombosis, Institute of Experimental Medicine IMEX, National Academy of Medicine, Buenos Aires, Argentina
    FASEB J 26:2788-98. 2012
    ..This study identifies a noncanonical mechanism, based on galectin-integrin interactions, for regulating platelet activation...
  12. pmc Prostacyclin prevents nitric oxide-induced megakaryocyte apoptosis
    Roberto Gabriel Pozner
    Department of Thrombosis and Haemostasis, Hematological Research Institute, National Academy of Medicine, National Research Council CONICET, Pacheco de Melo 3081 1425, Buenos Aires, Argentina
    Br J Pharmacol 145:283-92. 2005
    ....
  13. doi request reprint Identification of galectins as novel regulators of platelet signaling and function
    Maria Albertina Romaniuk
    Thrombosis I Laboratory, National Academy of Medicine, CONICET, Argentina
    IUBMB Life 63:521-7. 2011
    ..We also offer new hypotheses and some speculations about the role of platelet-galectin interactions not only in hemostasis and thrombosis but also in inflammation and related diseases such as atherosclerosis and cancer...
  14. doi request reprint Galectins: new agonists of platelet activation
    Mirta Schattner
    Laboratory of Experimental Thrombosis, Institute of Experimental Medicine IMEX CONICET, National Academy of Medicine, C1425, Buenos Aires, Argentina
    Biol Chem 394:857-63. 2013
    ..We discuss the role of platelet-galectin interactions not only in hemostasis, but also in chronic inflammation, atherosclerosis and cancer...
  15. pmc Control of angiogenesis by galectins involves the release of platelet-derived proangiogenic factors
    Julia Etulain
    Laboratory of Experimental Thrombosis, Institute of Experimental Medicine, CONICET National Academy of Medicine, Buenos Aires, Argentina
    PLoS ONE 9:e96402. 2014
    ....
  16. ncbi request reprint Differential astrocyte response to Theiler's murine encephalomyelitis virus infection
    Roberto G Pozner
    Department of Thrombosis and Haemostasis, Hematological Research Institute, National Academy of Medicine, University of Buenos Aires, Buenos Aires, Argentina
    Intervirology 48:279-84. 2005
    ..In addition, we investigated whether L*-1-infected astrocytes were able to selectively express molecules whose effects would play a role as pathogenic factors...
  17. ncbi request reprint Regulation of platelet responses triggered by Toll-like receptor 2 and 4 ligands is another non-genomic role of nuclear factor-kappaB
    Leonardo Rivadeneyra
    Laboratory of Experimental Thrombosis, Institute of Experimental Medicine CONICET, National Academy of Medicine, Buenos Aires, Argentina
    Thromb Res 133:235-43. 2014
    ..The aim of this study was to determine whether NF-κB activation is a downstream signal involved in TLR2 and 4-mediated platelet responses...
  18. ncbi request reprint Decreased beta-adrenoceptor chronotropic response in selenium-deficient mice: negative crosstalk between iNOS activity and cAMP accumulation
    Ricardo M Gomez
    Catedra de Farmacologia, Facultad de Odontologia, Universidad de Buenos Aires, Buenos Aires, 1122, Argentina
    Biol Trace Elem Res 117:127-38. 2007
    ....
  19. ncbi request reprint The snake venom metalloproteases berythractivase and jararhagin activate endothelial cells
    Mirta Schattner
    Department of Thrombosis and Hemostasis, National Academy of Medicine, National Research Council CONICET, 1425 Buenos Aires, Argentina
    Biol Chem 386:369-74. 2005
    ..Although structurally related, berythractivase and jararhagin induce a dissimilar generation and release of endothelial molecules that may account for their different hemorrhagic activity...
  20. ncbi request reprint Characterization of LIC11207, a novel leptospiral protein that is recognized by human convalescent sera and prevents apoptosis of polymorphonuclear leukocytes
    Gabriela Pretre
    Instituto de Biotecnologia y Biologia Molecular, CONICET, Facultad de Ciencias Exactas, Universidad Nacional de La Plata, Argentina
    Microb Pathog 56:21-8. 2013
    ..Interestingly, rLIC11207 delayed apoptosis of PMNs suggesting a possible role of this protein during the infection...
  21. doi request reprint Human platelets express and are activated by galectin-8
    Maria Albertina Romaniuk
    Thrombosis I Laboratory, Hematological Research Institute, National Academy of Medicine, CONICET, Buenos Aires, Argentina
    Biochem J 432:535-47. 2010
    ..These findings reveal Gal-8 as a potent platelet activator, supporting a role for this lectin in thrombosis and inflammation...
  22. ncbi request reprint Endothelial cell function alteration after Junin virus infection
    Ricardo Martin Gomez
    Department of Microbiology, Faculty of Medicine, University of Buenos Aires, CONICET, Argentina
    Thromb Haemost 90:326-33. 2003
    ..These data demonstrate that endothelial cell responses are triggered subsequently by JV infection, suggesting that such alterations play a major role in the pathogenesis of AHF and perhaps in other viral-induced hemorrhagic diseases...