ADAM17-deficiency on microglia but not on macrophages promotes phagocytosis and functional recovery after spinal cord injury.
ADAM17
Inflammation
Macrophages
Microglia
Spinal cord injury
Journal
Brain, behavior, and immunity
ISSN: 1090-2139
Titre abrégé: Brain Behav Immun
Pays: Netherlands
ID NLM: 8800478
Informations de publication
Date de publication:
08 2019
08 2019
Historique:
received:
11
12
2018
revised:
12
02
2019
accepted:
27
02
2019
pubmed:
10
3
2019
medline:
2
6
2020
entrez:
10
3
2019
Statut:
ppublish
Résumé
A disintegrin and metalloproteinase 17 (ADAM17) is the major sheddase involved in the cleavage of a plethora of cytokines, cytokine receptors and growth factors, thereby playing a substantial role in inflammatory and regenerative processes after central nervous system trauma. By making use of a hypomorphic ADAM17 knockin mouse model as well as pharmacological ADAM10/ADAM17 inhibitors, we showed that ADAM17-deficiency or inhibition significantly increases clearance of apoptotic cells, promotes axon growth and improves functional recovery after spinal cord injury (SCI) in mice. Microglia-specific ADAM17-knockout (ADAM17flox
Identifiants
pubmed: 30851378
pii: S0889-1591(18)31201-7
doi: 10.1016/j.bbi.2019.02.032
pii:
doi:
Substances chimiques
ADAM17 Protein
EC 3.4.24.86
Adam17 protein, mouse
EC 3.4.24.86
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
129-145Informations de copyright
Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.