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Tytuł pozycji:

Amyloid precursor protein binds with TNFRSF21 to induce neural inflammation in Alzheimer's Disease.

Tytuł:
Amyloid precursor protein binds with TNFRSF21 to induce neural inflammation in Alzheimer's Disease.
Autorzy:
Zhang T; Department of Rehabilitation, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China. Electronic address: .
Yu J; Department of Rehabilitation, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Wang G; Department of Rehabilitation, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Zhang R; Department of Rehabilitation, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Źródło:
European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences [Eur J Pharm Sci] 2021 Feb 01; Vol. 157, pp. 105598. Date of Electronic Publication: 2020 Oct 16.
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Publication: Amsterdam : Elsevier Science B.V
Original Publication: Amsterdam ; New York : Elsevier, c1993-
MeSH Terms:
Alzheimer Disease*
Amyloid beta-Protein Precursor*/genetics
Amyloid beta-Protein Precursor*/metabolism
Amyloid beta-Peptides/metabolism ; Animals ; Brain/metabolism ; Disease Models, Animal ; Inflammation ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic
Substance Nomenclature:
0 (Amyloid beta-Peptides)
0 (Amyloid beta-Protein Precursor)
Entry Date(s):
Date Created: 20201019 Date Completed: 20210621 Latest Revision: 20210621
Update Code:
20240105
DOI:
10.1016/j.ejps.2020.105598
PMID:
33075465
Czasopismo naukowe
Objects: Several evidences suggested that TNFRSF21 exert crucial functions in regulating neuroinflammatory effects, which had been detected in Alzheimer's Disease (AD). We performed many experiments aimed to explore the comprehensively biological functions of TNFRSF21 and its underlying mechanism in AD.
Methods: Twelve normal healthy C57BL6 mice were selected, and AD model mice (APP transgenic model Tg2576 and Tau transgenic model JNPL3) were constructed and TNFRSF21 knockdown was performed in vitro. Western blotting, Co-immunoprecipitation (Co-IP), ELISA assay, flow cytometry and immunofluorescence were performed to explore the biological functions of APP and its underlying mechanism in AD.
Results: The expression of TNFRSF21, APP, NF-κB and MAPK8 was increased in APP transgenic model (Tg2576) and Tau transgenic model (JNPL3). The interaction between TNFRSF21 and APP was analyzed by Co-IP at protein level. Based on the results of ELISA, the levels of inflammatory cytokines TNF-α, IL-5, and IFN-γ in the Tg2576 were higher than that in the JNPL3, but hardly observed in the normal group. The increased APP and inflammatory cytokines in AD model were significantly reduced with TNFRSF21 inhibited. Tg2576 group exhibited higher apoptotic rate of neuron cell and increased number of astrocytes than those of the JNPL3 group.
Conclusions: Our studies revealed that APP could promote and bind with TNFRSF21 to regulate the neural inflammatory effects in AD. Inhibiting TNFRSF21 could reduce APP expression and decrease neuroinflammation, which might become potential target for treating AD.
(Copyright © 2020. Published by Elsevier B.V.)

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