Abstract
It was not clear how and whether neural stem cells (NSCs) responded to toll-like receptor 2 (TLR2) in the inflammatory environment after traumatic brain injury (TBI). The current study investigated the correlation of TLR2 and NSC proliferation in the dentate gyrus (DG) using the TBI model of rats. Immunofluorescence (IF) was used to observe the expression of BrdU, nestin, and TLR2 in the DG in morphology. Proliferating cells in the DG were labelled by thymidine analog 5-bromo-2-deoxyuridine (BrdU). Three-labelled BrdU, nestin, and DAPI was used for the identification of newly generated NSCs. Western blotting and real-time polymerase chain reaction (PCR) were used to observe the expression of TLR2 from the level of protein and mRNA. We observed that BrdU+/nestin+/DAPI+ cells accounted for 84.30% ± 6.54% among BrdU+ cells; BrdU+ and nestin+ cells in the DG were also TLR2+ cells. BrdU+ cells and the expression of TLR2 (both protein and mRNA levels) both elevated immediately at 6 hours (h), 24 h, 3 days (d), and 7 d posttrauma and peaked in 3 d. Results indicated that TLR2 was expressed on proliferating cells in the DG (NSCs possibly) and there was a potential correlation between increased TLR2 and proliferated NSCs after TBI. Taken together, these findings suggested that TLR2 was involved in endogenous neurogenesis in the DG after TBI.
Highlights
Neurogenesis occurs in the immature brain and in the mature brain of mammals
It is well known that neural stem cells (NSCs) exist mainly in two regions of the adult brain—the subgranular zone (SGZ) of the hippocampal dentate gyrus (DG) [2] and the subventricular zone (SVZ) of lateral ventricles [3]
Many studies have demonstrated that endogenous neurogenesis in the adult brain can be regulated by inflammatory reaction after neural trauma [9,10,11], it is still not clear how the inflammation within the brain influences the process of neurogenesis through NSC proliferation, differentiation, migration, and integration after traumatic brain injury (TBI)
Summary
Neurogenesis occurs in the immature brain and in the mature brain of mammals. It is well known that NSCs exist mainly in two regions of the adult brain—the subgranular zone (SGZ) of the hippocampal dentate gyrus (DG) [2] and the subventricular zone (SVZ) of lateral ventricles [3]. Cells in these regions have potential self-renewal capacity and can turn out to become newborn neurons, microglia, oligodendrocytes, and astrocytes [4]. Many studies have demonstrated that endogenous neurogenesis in the adult brain can be regulated by inflammatory reaction after neural trauma [9,10,11], it is still not clear how the inflammation within the brain influences the process of neurogenesis through NSC proliferation, differentiation, migration, and integration after traumatic brain injury (TBI)
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