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Journal of Biomedicine and Biotechnology
Volume 2010 (2010), Article ID 137817, 13 pages
Research Article

Epo Is Relevant Neither for Microvascular Formation Nor for the New Formation and Maintenance of Mice Skeletal Muscle Fibres in Both Normoxia and Hypoxia

1Laboratoire “Réponses Cellulaires et Fonctionnelles à l'hypoxie”, Université Paris 13, EA 2363, 97017 Bobigny, France
2Laboratoire Stress et Pathologies du Cytosquelette, Unité de Biologie Adaptative et Fonctionnelle, Université Paris Diderot-Paris 7 CNRS, 75013 Paris, France
3Université Paris-Descartes, 75015 Paris, France

Received 30 October 2009; Revised 28 January 2010; Accepted 9 February 2010

Academic Editor: Aikaterini Kontrogianni-Konstantopoulos

Copyright © 2010 Luciana Hagström et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Erythropoietin (Epo) and vascular growth factor (VEGF) are known to be involved in the regulation of cellular activity when oxygen transport is reduced as in anaemia or hypoxic conditions. Because it has been suggested that Epo could play a role in skeletal muscle development, regeneration, and angiogenesis, we aimed to assess Epo deficiency in both normoxia and hypoxia by using an Epo-deficient transgenic mouse model ( E p o - T A g h ). Histoimmunology, ELISA and real time RT-PCR did not show any muscle fiber atrophy or accumulation of active HIF-1 𝛼 but an improvement of microvessel network and an upregulation of VEGFR2 mRNA in Epo-deficient gastrocnemius compared with Wild-Type one. In hypoxia, both models exhibit an upregulation of VEGF120 and VEGFR2 mRNA but no accumulation of Epo protein. EpoR mRNA is not up-regulated in both Epo-deficient and hypoxic gastrocnemius. These results suggest that muscle deconditioning observed in patients suffering from renal failure is not due to Epo deficiency.