1. HIF-1α expression in the hippocampus and peripheral macrophages after glutamate-induced excitotoxicity.
- Author
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Vazquez-Valls E, Flores-Soto ME, Chaparro-Huerta V, Torres-Mendoza BM, Gudiño-Cabrera G, Rivera-Cervantes MC, Pallas M, Camins A, Armendáriz-Borunda J, and Beas-Zarate C
- Subjects
- Age Factors, Animals, Animals, Newborn, Disease Models, Animal, Erythropoietin genetics, Erythropoietin metabolism, Female, Gene Expression Regulation, Developmental drug effects, Glial Fibrillary Acidic Protein metabolism, Glutamic Acid toxicity, Hippocampus drug effects, Hippocampus pathology, Hypoxia-Inducible Factor 1, alpha Subunit genetics, Macrophages drug effects, Male, Neurons drug effects, Neurons metabolism, Neurotoxicity Syndromes etiology, Neurotoxins toxicity, Pregnancy, RNA, Messenger, Rats, Rats, Wistar, Vascular Endothelial Growth Factor A genetics, Vascular Endothelial Growth Factor A metabolism, Gene Expression Regulation, Developmental physiology, Hippocampus metabolism, Hypoxia-Inducible Factor 1, alpha Subunit metabolism, Macrophages metabolism, Neurotoxicity Syndromes pathology
- Abstract
Hypoxia-inducible factor-1 alpha (HIF-1α) is a master transcription factor that regulates the response to hypoxia and ischemia and induces the expression of various genes, including vascular endothelial growth factor (VEGF) and erythropoietin (EPO). This study shows the systemic response of increased HIF-1α, EPO, and VEGF mRNA and protein. In addition, VEGF expression was increased in neurons and over-expressed in glial cells in a model of neuroexcitotoxicity in the hippocampus, in which rats were neonatally exposed to high glutamate concentrations. Simultaneous increases in HIF-1α, EPO and VEGF mRNA in peritoneal macrophages were also observed. Our study is consistent with the hypothesis that these genes exert a protective effect in response to neurotoxicity., (Copyright © 2011 Elsevier B.V. All rights reserved.)
- Published
- 2011
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