Dynamics of PDGFRβ Expression in Different Cell Types after Brain Injury

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