Upregulation of IFN-β induced by Sema4D-dependent partial Erk1/2 inhibition promotes NO production in microglia.
Animals
Antigens, CD
/ metabolism
Antigens, Differentiation, B-Lymphocyte
/ metabolism
Brain Ischemia
/ metabolism
Cells, Cultured
Flavonoids
/ pharmacology
Interferon-beta
/ genetics
Lipopolysaccharides
/ pharmacology
Mice, Inbred C57BL
Mice, Knockout
Microglia
/ drug effects
Mitogen-Activated Protein Kinase 1
/ antagonists & inhibitors
Mitogen-Activated Protein Kinase 3
/ antagonists & inhibitors
Nerve Tissue Proteins
/ metabolism
Nitric Oxide
/ metabolism
Phosphorylation
Receptors, Cell Surface
/ metabolism
Semaphorins
/ genetics
Up-Regulation
Erk1/2
IFN-β
Microglia
NO
Sema4D
Journal
Biochemical and biophysical research communications
ISSN: 1090-2104
Titre abrégé: Biochem Biophys Res Commun
Pays: United States
ID NLM: 0372516
Informations de publication
Date de publication:
22 01 2020
22 01 2020
Historique:
received:
21
10
2019
accepted:
31
10
2019
pubmed:
12
11
2019
medline:
4
8
2020
entrez:
12
11
2019
Statut:
ppublish
Résumé
Interactions between Sema4D and its receptors, PlexinB1 and CD72, induce various functions, including axon guidance, angiogenesis, and immune activation. Our previous study revealed that Sema4D is involved in the upregulation of nitric oxide production in microglia after cerebral ischemia. In this study, we investigated the underlying mechanisms of the enhancement of microglial nitric oxide production by Sema4D. Primary microglia expressed PlexinB1 and CD72, and cortical microglia expressed CD72. Sema4D promoted nitric oxide production and slightly inhibited Erk1/2 phosphorylation in microglia. Partial Erk1/2 inhibition enhanced microglial nitric oxide production. Inhibition of Erk1/2 phosphorylation induced the expression of Ifn-β mRNA, and IFN-β promoted nitric oxide production in microglia. In the ischemic cortex, the expression of Ifn-β mRNA was downregulated by Sema4D deficiency. These findings indicated that the enhancement of nitric oxide production by Sema4D is involved in partial Erk1/2 inhibition and upregulation of IFN-β.
Identifiants
pubmed: 31708102
pii: S0006-291X(19)32117-5
doi: 10.1016/j.bbrc.2019.10.201
pii:
doi:
Substances chimiques
Antigens, CD
0
Antigens, Differentiation, B-Lymphocyte
0
CD72 antigen, mouse
0
Flavonoids
0
Lipopolysaccharides
0
Nerve Tissue Proteins
0
Plxnb1 protein, mouse
0
Receptors, Cell Surface
0
Sema4d protein, mouse
0
Semaphorins
0
Nitric Oxide
31C4KY9ESH
Interferon-beta
77238-31-4
Mapk1 protein, mouse
EC 2.7.11.24
Mapk3 protein, mouse
EC 2.7.11.24
Mitogen-Activated Protein Kinase 1
EC 2.7.11.24
Mitogen-Activated Protein Kinase 3
EC 2.7.11.24
2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one
SJE1IO5E3I
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
827-832Informations de copyright
Copyright © 2019. Published by Elsevier Inc.