Article Dans Une Revue Respiratory physiology & neurobiology Année : 2013

Epo deficiency alters cardiac adaptation to chronic hypoxia.

Raja El Hasnaoui-Saadani
  • Fonction : Auteur
Dominique Marchant
  • Fonction : Auteur
Aurélien Pichon
Brigitte Escoubet
  • Fonction : Auteur
Mylène Pezet
  • Fonction : Auteur
Denise Hilfiker-Kleiner
  • Fonction : Auteur
Melanie Hoch
  • Fonction : Auteur
Isabelle Pham
  • Fonction : Auteur
Patricia Quidu
  • Fonction : Auteur
Nicolas Voituron
  • Fonction : Auteur
Clément Journé
  • Fonction : Auteur
Jean-Paul Richalet
  • Fonction : Auteur

Résumé

The involvement of erythropoietin in cardiac adaptation to acute and chronic (CHx) hypoxia was investigated in erythropoietin deficient transgenic (Epo-TAg(h)) and wild-type (WT) mice. Left (LV) and right ventricular functions were assessed by echocardiography and hemodynamics. HIF-1α, VEGF and Epo pathways were explored through RT-PCR, ELISA, Western blot and immunocytochemistry. Epo gene and protein were expressed in cardiomyocytes of WT mice in normoxia and hypoxia. Increase in blood hemoglobin, angiogenesis and functional cardiac adaptation occurred in CHx in WT mice, allowing a normal oxygen delivery (O2T). Epo deficiency induced LV hypertrophy, increased cardiac output (CO) and angiogenesis, but O2T remained lower than in WT mice. In CHx Epo-TAg(h) mice, LV hypertrophy, CO and O2T decreased. HIF-1α and Epo receptor pathways were depressed, suggesting that Epo-TAg(h) mice could not adapt to CHx despite activation of cardioprotective pathways (increased P-STAT-5/STAT-5). HIF/Epo pathway is activated in the heart of WT mice in hypoxia. Chronic hypoxia induced cardiac adaptive responses that were altered with Epo deficiency, failing to maintain oxygen delivery to tissues.

Dates et versions

hal-05259040 , version 1 (15-09-2025)

Identifiants

Citer

Raja El Hasnaoui-Saadani, Dominique Marchant, Aurélien Pichon, Brigitte Escoubet, Mylène Pezet, et al.. Epo deficiency alters cardiac adaptation to chronic hypoxia.. Respiratory physiology & neurobiology, 2013, 186 (2), pp.146-154. ⟨10.1016/j.resp.2013.01.003⟩. ⟨hal-05259040⟩
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