作者: Jenni Kyyriäinen , Xavier Ekolle Ndode-Ekane , Asla Pitkänen
DOI: 10.1002/GLIA.23094
关键词:
摘要: Platelet-derived growth factor receptor β (PDGFRβ) is upregulated after brain injury and its depletion results in the blood–brain barrier (BBB) damage. We investigated time-window localization of PDGFRβ expression mice with intrahippocampal kainic acid-induced status epilepticus (SE) rats lateral fluid-percussion-induced traumatic (TBI). Tissue immunohistochemistry was evaluated at several time-points SE TBI. The distribution analyzed, cell type-specific verified double/triple-labeling astrocytes (GFAP), NG2 cells, endothelial cells (RECA-1). In normal mouse hippocampus, we found evenly distributed PDGFRβ+ parenchymal cells. double-labeling, all NG2+ 40%–60% GFAP+ were PDGFRβ+. After SE, clustered ipsilateral hilus (178% that controls fourth day, 225% seventh P < 0.05) CA3 (201% P < 0.05), but total number not altered. As controls, PDGFRβ-immunoreactivity detected also observed structural pericytes, detached reactive TBI, perilesional cortex thalamus, particularly during first post-injury week. immunopositivity some animals, vascular staining around cortical glial scar for up to 3 months. Our data revealed an acute accumulation BBB-related degenerating areas, which can be long lasting, suggesting active role PDGFRβ-signaling blood vessel tissue recovery. GLIA 2016