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Since cardiac progenitor cells are considered a regenerative cell source upon cardiac injury, the protective action of the EPO system was tested by creating an erythroid-rescued EPOR knockout mouse model.
In this article, we review probable contributions of the nonclassical EPO system to physiologic conditions associated with severe illness.
As compared to neuroprotection studies in disease models (for review see [ 12]), work on the function of the EPO system in normal brain is scarce.
A potential explanation for the cEPOR TG phenotype of impulsivity and hyperactivity might be the continuous stimulation of the EPO system exclusively in cortical projection neurons.
This way, we were able to specifically mimic EPO system function independent of any ligand in pyramidal neurons of cortex and hippocampus, that is regions pivotal for learning and memory processes.
In other words, we 'over-accentuated' the endogenous action of the EPO system in specific cortical and hippocampal layers, particularly the CA1 subregion [ 28], to delineate the contribution of these neuronal subpopulations to the EPO effects on cognition.
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Frozen plasma was transported to the UK for the analysis of ferritin (Imx ferritin assay based on Microparticle Enzyme Immunoassay (MEIA) technology, Abbot Laboratories), soluble transferrin receptors (STfR) (R&D systems ELISA), erythropoetin (Epo) (R&D systems Quantikine IVD ELISA) and C reactive protein (CRP)(Dade Dimension particle enhanced turbidimetric immunoassay).
The importance of the EPO-EPOR system in erythropoiesis and vasculogenesis was established using mutant mice lacking either the Epo or EpoR gene [38].
Markers (HIF-2 α, VEGF, EPO, EPO-R, Glut-1, and Ki-67) in the carcinogenesis study were scored using the same scoring system.
Thus, our current findings suggest that the EPO-EPOR system may constitute a potential target for the therapeutic modulation of angiogenesis in cancer that warrants further investigation.
Wang W et al. documented that the EPO-EPOR system mediated accelerated phosphorylation of STAT3, Akt and eNOS and depressed phosphorylation of p38, resulting in prevention of myocardial fibrosis [ 7].
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