Please use this identifier to cite or link to this item: http://hdl.handle.net/2445/55583
Title: Glucose pathways adaptation supports acquisition of activated microglia phenotype
Author: Gimeno-Bayon, Javier
López-López, A.
Rodríguez Allué, Manuel José
Mahy Gehenne, Josette Nicole
Keywords: Glucòlisi
Pentoses
Òxid nítric
Micròglia
Glycolysis
Pentoses
Nitric oxide
Microglia
Issue Date: 7-Feb-2014
Publisher: Wiley
Abstract: With its capacity to survey the environment and phagocyte debris, microglia assume a diversity of phenotypes to respond specifically through neurotrophic and toxic effects. Although these roles are well accepted, the underlying energetic mechanisms associated with microglial activation remain largely unclear. This study investigates microglia metabolic adaptation to ATP, NADPH, H(+) , and reactive oxygen species production. To this end, in vitro studies were performed with BV-2 cells before and after activation with lipopolysaccharide + interferon-γ. Nitric oxide (NO) was measured as a marker of cell activation. Our results show that microglial activation triggers a metabolic reprogramming based on an increased glucose uptake and a strengthening of anaerobic glycolysis, as well as of the pentose pathway oxidative branch, while retaining the mitochondrial activity. Based on this energy commitment, microglial defense capacity increases rapidly as well as ribose-5-phosphate and nucleic acid formation for gene transcription, essential to ensure the newly acquired functions demanded by central nervous system signaling. We also review the role of NO in this microglial energy commitment that positions cytotoxic microglia within the energetics of the astrocyte-neuron lactate shuttle.
Note: Versió postprint del document publicat a: http://dx.doi.org/10.1002/jnr.23356
It is part of: Journal of Neuroscience Research, 2014, vol. 92, num. 6, p. 723-731
Related resource: http://dx.doi.org/10.1002/jnr.23356
URI: http://hdl.handle.net/2445/55583
ISSN: 0360-4012
Appears in Collections:Articles publicats en revistes (Ciències Fisiològiques)

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