Abstract
Erythropoietin (Epo) and vascular growth factor (VEGF) are known to be involved in the regulation of cellular activity when oxygen transport is reduced like in anemia or hypoxic conditions. Because it has been suggested that Epo could have a role in skeletal muscle development, repair and angiogenesis we aimed to assess Epo‐deficiency using Epo‐deficient trangenic (Epo‐TAgh) mouse model in both normoxia and hypoxia. By histoimmunology, ELISA and real time PCR we did not observe any muscle fibre atrophy or accumulation of active HIF1‐α but an improvement of microvessel network and an up‐regulation of VEGFR2 mRNA in Epo‐deficent gastrocnemius compare to wild type one. In hypoxia both models exhibit an up‐regulation of VEGF120 and VEGFR2 mRNA but no accumulation of Epo protein. EpoR mRNA is not up‐regulated in both Epo‐deficient and hypoxic gastrocnemius. In conclusion muscle deconditioning observed in patients suffering from renal failure are not due to Epo‐deficency.
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