Characterization of Gcf2/Lrrfip1 in experimental cerebral ischemia and its role as a modulator of Akt, mTOR and β-catenin signaling pathways

Highlights • At least five transcriptional variants of Lrrfip1 are expressed in the rat brain. • Brain ischemia up-regulates Lrrfip1 transcripts with different expression patterns. • Our results suggest that distinct Lrrfip1 isoforms can play different roles. • rLrrfip1 activates β-catenin, Akt and...

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Veröffentlicht in:	Neuroscience 2014-05, Vol.268, p.48-65
Hauptverfasser:	Gubern, C, Camós, S, Hurtado, O, Rodríguez, R, Romera, V.G, Sobrado, M, Cañadas, R, Moro, M.A, Lizasoain, I, Serena, J, Mallolas, J, Castellanos, M
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals astrocytes Astrocytes - metabolism beta Catenin - metabolism Biological and medical sciences Brain - metabolism Brain Ischemia - etiology Brain Ischemia - metabolism Cells, Cultured Cytoplasm - metabolism Excitatory Amino Acid Transporter 2 - metabolism Fundamental and applied biological sciences. Psychology Gene Knockdown Techniques GLT-1 Glutamic Acid - metabolism Infarction, Middle Cerebral Artery - complications Infarction, Middle Cerebral Artery - metabolism Lrrfip1 Male MCAO Medical sciences Neurology Neurons - metabolism OGD Proto-Oncogene Proteins c-akt - metabolism Rats, Inbred F344 Rats, Wistar RNA Isoforms - metabolism RNA-Binding Proteins - genetics RNA-Binding Proteins - metabolism Signal Transduction stroke TOR Serine-Threonine Kinases - metabolism Up-Regulation Vascular diseases and vascular malformations of the nervous system Vertebrates: nervous system and sense organs
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Zusammenfassung:	Highlights • At least five transcriptional variants of Lrrfip1 are expressed in the rat brain. • Brain ischemia up-regulates Lrrfip1 transcripts with different expression patterns. • Our results suggest that distinct Lrrfip1 isoforms can play different roles. • rLrrfip1 activates β-catenin, Akt and mTOR proteins in astrocytes. • rLrrfip1 knockdown reduces GLT-1 expression and glutamate uptake in astrocytes.
ISSN:	0306-4522 1873-7544
DOI:	10.1016/j.neuroscience.2014.02.051