Hindawi Publishing Corporation
Journal of Biomedicine and Biotechnology
Volume 2010, Article ID 137817, 13 pages
doi:10.1155/2010/137817
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
Luciana Hagström,1 Onnik Agbulut,2 Raja El-Hasnaoui-Saadani,1 DominiqueMarchant,1
Fabrice Favret,1 Jean-Paul Richalet,1 Michèle Beaudry,1 and Thierry Launay1, 3
1 Laboratoire “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
Correspondence should be addressed to Thierry Launay, thy.launay@free.fr
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 (Epo-TAgh). Histoimmunology, ELISA and real time RT-PCR did not show
any muscle fiber atrophy or accumulation of active HIF-1α 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