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Acta Academiae Medicinae Sinicae ; (6): 217-221, 2016.
Article in Chinese | WPRIM | ID: wpr-289878

ABSTRACT

<p><b>OBJECTIVE</b>To explore the impacts of erythropoietin on vascular endothelial growth factor receptor 2 (VEGFR2) by the extracellular signal-regulated kinase (ERK) signaling pathway in a neonatal rat model of periventricular white matter damage.</p><p><b>METHODS</b>All of postnatal day 4 rats were randomized into three groups: the sham group [without hypoxia-ischemia (HI)], the HI group (HI with saline administration), and the erythropoietin (EPO) group [HI with recombinant human erythropoietin (rh-EPO) administration]. Rat pups underwent permanent ligation of the right common carotid artery, followed by 6% O2 for 2 hours or sham operation and normoxic exposure. Immediately after the HI, rats received a single intraventricular injection of rh-EPO (0.6 IU/g body mass) or saline. ERK and phosphorylation-ERK were examined at 60 minutes and 90 minutes after operation, and VEGFR2 were detected at 2 and 4 days after operation by using Western blot.</p><p><b>RESULTS</b>At 60 minutes and 90 minutes after operation, the proteins of phosphorylation-ERK were significantly higher in HI rats than in the sham rats and significantly higher in HI+EPO rats than in the HI rats (P<0.05). Two days after operation, VEGFR2 was not significantly different between sham and HI rats. However, the proteins of VEGFR2 were increased after administration of rh-EPO (P<0.05). Four days after operation, the proteins of VEGFR2 were significantly higher in HI rats than in the sham rats and significantly higher in HI+EPO rats than in the HI rats (P<0.05).</p><p><b>CONCLUSION</b>EPO may regulate VEGFR2 expression by affecting the intracranial ERK signaling pathways.</p>


Subject(s)
Animals , Humans , Rats , Animals, Newborn , Disease Models, Animal , Erythropoietin , Pharmacology , Hypoxia-Ischemia, Brain , MAP Kinase Signaling System , Phosphorylation , Rats, Sprague-Dawley , Recombinant Proteins , Pharmacology , Vascular Endothelial Growth Factor Receptor-2 , Metabolism , White Matter
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