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<dc:title>Apolipoprotein D alters the early transcriptional response to oxidative stress in the adult cerebellum</dc:title>
<dc:creator>Bajo Grañeras, Raquel</dc:creator>
<dc:creator>Sánchez Romero, Diego</dc:creator>
<dc:creator>Gutiérrez, Gabriel</dc:creator>
<dc:creator>González Martínez, Constancio</dc:creator>
<dc:creator>Carmo, Sonia do</dc:creator>
<dc:creator>Rassart, Eric</dc:creator>
<dc:creator>Ganfornina Álvarez, María Dolores</dc:creator>
<dc:subject>Nervioso, sistema - Fisiología</dc:subject>
<dc:description>Producción Científica</dc:description>
<dc:description>The lipocalin Apolipoprotein D (ApoD), known to protect the&#xd;
nervous system against oxidative stress (OS) in model&#xd;
organisms, is up-regulated early in the mouse brain in&#xd;
response to the ROS generator paraquat. However, the processes&#xd;
triggered by this up-regulation have not been explored.&#xd;
We present here a study of the effect of ApoD on the early&#xd;
transcriptional changes upon OS in the mouse cerebellum&#xd;
using microarray profiling. ApoD-KO and transgenic mice&#xd;
over-expressing ApoD in neurons are compared to wild-type&#xd;
controls. In control conditions, ApoD affects the transcriptional&#xd;
profile of neuron and oligodendrocyte-specific genes involved&#xd;
in neuronal excitability, synaptic function, and myelin&#xd;
homeostasis. When challenged with paraquat, the absence of&#xd;
ApoD modifies the response of genes mainly related to OS&#xd;
management and myelination. Interestingly, the over-expression&#xd;
of ApoD in neurons almost completely abolishes the early&#xd;
transcriptional response to OS. We independently evaluate&#xd;
the expression of protein kinase Cd, a gene up-regulated by&#xd;
OS only in the ApoD-KO cerebellum, and find it overexpressed&#xd;
in cultured ApoD-KO primary astrocytes, which&#xd;
points to a role for ApoD in astrocyte-microglia signaling. Our&#xd;
results support the hypothesis that ApoD is necessary for a&#xd;
proper response of the nervous system against physiological&#xd;
and pathological OS.</dc:description>
<dc:description>2015-09-19</dc:description>
<dc:date>2014-09-19T16:34:44Z</dc:date>
<dc:date>2015-09-19T23:40:08Z</dc:date>
<dc:date>2011</dc:date>
<dc:type>info:eu-repo/semantics/article</dc:type>
<dc:identifier>Journal of Neurochemistry, 2011, vol. 117, p. 949-960</dc:identifier>
<dc:identifier>0022-3042</dc:identifier>
<dc:identifier>http://uvadoc.uva.es/handle/10324/6099</dc:identifier>
<dc:identifier>10.1111/j.1471-4159.2011.07266.x</dc:identifier>
<dc:identifier>949</dc:identifier>
<dc:identifier>960</dc:identifier>
<dc:identifier>Journal of Neurochemistry</dc:identifier>
<dc:identifier>117</dc:identifier>
<dc:language>eng</dc:language>
<dc:rights>Attribution-NonCommercial-NoDerivatives 4.0 International</dc:rights>
<dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
<dc:rights>http://creativecommons.org/licenses/by-nc-nd/4.0/</dc:rights>
<dc:format>application/pdf</dc:format>
<dc:publisher>International Society for Neurochemistry</dc:publisher>
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