Toll-Like Receptor 2 Attenuates Traumatic Brain Injury-Induced Neural Stem Cell Proliferation in Dentate Gyrus of Rats.

Publisher: Hindawi Pub. Corp Country of Publication: United States NLM ID: 100883417 Publication Model: eCollection Cited Medium: Internet ISSN: 1687-5443 (Electronic) Linking ISSN: 16875443 NLM ISO Abbreviation: Neural Plast Subsets: MEDLINE

Publication: New York, NY : Hindawi Pub. Corp
Original Publication: Patrington, East Yorkshire, U.K. : Freund & Pettman, c1998-

Cell Proliferation* ; Neurogenesis*; Brain Injuries, Traumatic/*physiopathology ; Dentate Gyrus/*physiopathology ; Neural Stem Cells/*physiology ; Toll-Like Receptor 2/*physiology; Animals ; Brain Injuries, Traumatic/metabolism ; Brain Injuries, Traumatic/pathology ; Dentate Gyrus/metabolism ; Dentate Gyrus/pathology ; Male ; RNA, Messenger/metabolism ; Rats, Sprague-Dawley ; Toll-Like Receptor 2/metabolism

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.
Competing Interests: The authors declare no conflicts of interest.
(Copyright © 2020 Xin Zhang et al.)

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0 (RNA, Messenger)
0 (Tlr2 protein, rat)
0 (Toll-Like Receptor 2)

Date Created: 20200904 Date Completed: 20210803 Latest Revision: 20210803

20221213

PMC7448220

10.1155/2020/9814978

32879625