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Erythropoietin recapitulates hemodynamic features of hypoxia-induced pulmonary hypertension in mice

Julien Becker, Emilie Peter-Thiebaut, Ghina Bou About, Lahcen El Fertak, Megane Denu, Hugues Jacobs, Patrick Reilly, Yann Herault, Laurent Monassier
European Respiratory Journal 2016 48: PA5097; DOI: 10.1183/13993003.congress-2016.PA5097
Julien Becker
1Institut Clinique de la Souris (ICS), Phenomin, ICS, IGBMC, CNRS, Inserm, Université de Strasbourg, Illkirch, France
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Emilie Peter-Thiebaut
1Institut Clinique de la Souris (ICS), Phenomin, ICS, IGBMC, CNRS, Inserm, Université de Strasbourg, Illkirch, France
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Ghina Bou About
1Institut Clinique de la Souris (ICS), Phenomin, ICS, IGBMC, CNRS, Inserm, Université de Strasbourg, Illkirch, France
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Lahcen El Fertak
1Institut Clinique de la Souris (ICS), Phenomin, ICS, IGBMC, CNRS, Inserm, Université de Strasbourg, Illkirch, France
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Megane Denu
1Institut Clinique de la Souris (ICS), Phenomin, ICS, IGBMC, CNRS, Inserm, Université de Strasbourg, Illkirch, France
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Hugues Jacobs
1Institut Clinique de la Souris (ICS), Phenomin, ICS, IGBMC, CNRS, Inserm, Université de Strasbourg, Illkirch, France
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Patrick Reilly
1Institut Clinique de la Souris (ICS), Phenomin, ICS, IGBMC, CNRS, Inserm, Université de Strasbourg, Illkirch, France
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Yann Herault
1Institut Clinique de la Souris (ICS), Phenomin, ICS, IGBMC, CNRS, Inserm, Université de Strasbourg, Illkirch, France
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Laurent Monassier
1Institut Clinique de la Souris (ICS), Phenomin, ICS, IGBMC, CNRS, Inserm, Université de Strasbourg, Illkirch, France
2Laboratoire de Neurobiologie et Pharmacologie Cardiovasculaire EA 7296, Faculté de Médecine, Strasbourg, France
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Abstract

Background: Pulmonary hypertension (PH) is characterized by increased pulmonary vascular resistance leading to right ventricular failure. Chronic hypoxia is a risk factor for PH. Otherwise, end-stage renal disease treated by haemodialysis is a risk factor for PH that occurs in 40% of the patients. Most of these last patients are treated with human recombinant erythropoietin (EPO) because of anaemia. Involvement of EPO itself as causative agent of PH is a controversial issue.

Aims: We investigated if EPO could by itself recapitulate all hemodynamic and morphologic features of hypoxia-induced pulmonary hypertension at similar level of increased haematocrit. As a secondary endpoint, we investigated whether endothelial progenitor cells, mobilized and implied in PH due to chronic hypoxia, could also be involved in EPO-induced PH.

Methods: 1st group: mice were treated with recombinant human EPO in normoxia during 2 weeks. 2nd group: mice were exposed to 2 weeks of hypoxia (10%). Control mice were placed in normoxic conditions. Blood analysis, echocardiography, right ventricular pressure, heart and lung histology and blood circulating endothelial progenitor cells were assessed after 2 weeks.

Results: 2 weeks exogenous EPO treatment causes PH with an important increase in pulmonary and right ventricular pressure but without inducing right ventricle hypertrophy and pulmonary artery remodelling. EPO provoked an increase in the blood mobilization of endothelial progenitor cells at a similar extent than hypoxia.

Conclusions: EPO recapitulates hemodynamic features of hypoxia-induced pulmonary hypertension in mice. Similarly to this last disease, EPO mobilizes cells that trigger PH.

  • Pulmonary hypertension
  • Pharmacology
  • Animal models
  • Copyright ©the authors 2016
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Erythropoietin recapitulates hemodynamic features of hypoxia-induced pulmonary hypertension in mice
Julien Becker, Emilie Peter-Thiebaut, Ghina Bou About, Lahcen El Fertak, Megane Denu, Hugues Jacobs, Patrick Reilly, Yann Herault, Laurent Monassier
European Respiratory Journal Sep 2016, 48 (suppl 60) PA5097; DOI: 10.1183/13993003.congress-2016.PA5097

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Erythropoietin recapitulates hemodynamic features of hypoxia-induced pulmonary hypertension in mice
Julien Becker, Emilie Peter-Thiebaut, Ghina Bou About, Lahcen El Fertak, Megane Denu, Hugues Jacobs, Patrick Reilly, Yann Herault, Laurent Monassier
European Respiratory Journal Sep 2016, 48 (suppl 60) PA5097; DOI: 10.1183/13993003.congress-2016.PA5097
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