Source:Brain Research Bulletin
Author(s): Dan Pei, Nan Liu, Dan Li, Hongjing Yan, Qiu-bo Wang, Yan Fang, Ling Xie, Hong-Peng Li
Brain injury leads to complex cellular and molecular interactions within the central nervous system. As the glial scar was a mechanical barrier to regeneration, inhibitory molecules in the forming scar and methods to overcome them have suggested molecular modification strategies to allow neuronal growth and functional regeneration. Here we investigated the roles of PDGFRβ signaling in regulating astrocyte reactivity and scar formation in mice following traumatic brain injury (TBI). The expression and distribution of phosphorylated PDGFRβ was analyzed, and its cell type-specific expression was verified with double labeling of astrocytes (GFAP), microglia (IBA1), oligodendrocyte precursor cells (OPC) (NG2) and leukocytes (CD45). We found PDGFRβ was activated around the injury site after TBI, and primarily expressed in astrocytes, microglia, OPC and leukocytes in the boundary of the lesion site, suggesting PDGFRβ was involved in glial scar formation. Then the PDGFR inhibitor (AG1296) was administered following TBI. Reactive astrocytes were significantly inhibited in AG1296-treated mice. Furthermore, AG1296-treatment attenuated reactive leukocytes, OPC and astrocytes and pronouncedly disrupted of glial scar formation after TBI. These findings prove that PDGFRβ signaling inhibited reactive astrocytes-mediated scar formation after TBI in mice.
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