Targeted deletions of complement lectin pathway genes improve outcome in traumatic brain injury, with MASP-2 playing a major role.
Animals
Brain
/ metabolism
Brain Injuries, Traumatic
/ genetics
Collectins
/ genetics
Complement C4b
/ metabolism
Complement Pathway, Mannose-Binding Lectin
/ genetics
Gene Deletion
Inflammation
/ genetics
Lectins
/ genetics
Mannose-Binding Lectin
/ genetics
Mannose-Binding Protein-Associated Serine Proteases
/ genetics
Mice
Mice, Knockout
Prognosis
Recovery of Function
/ genetics
Ficolins
Complement cascade
Lectin pathway
MBL-associated serine protease
Neuroinflammation
Neurological deficits
Pharmacological target
Traumatic brain injury
Journal
Acta neuropathologica communications
ISSN: 2051-5960
Titre abrégé: Acta Neuropathol Commun
Pays: England
ID NLM: 101610673
Informations de publication
Date de publication:
28 10 2020
28 10 2020
Historique:
received:
22
07
2020
accepted:
24
09
2020
entrez:
29
10
2020
pubmed:
30
10
2020
medline:
11
11
2021
Statut:
epublish
Résumé
The lectin pathway (LP) of complement activation is believed to contribute to brain inflammation. The study aims to identify the key components of the LP contributing to TBI outcome as possible novel pharmacological targets. We compared the long-term neurological deficits and neuropathology of wild-type mice (WT) to that of mice carrying gene deletions of key LP components after experimental TBI. WT or MASP-2 (Masp2
Identifiants
pubmed: 33115535
doi: 10.1186/s40478-020-01041-1
pii: 10.1186/s40478-020-01041-1
pmc: PMC7592565
doi:
Substances chimiques
Colec11 protein, mouse
0
Collectins
0
Lectins
0
Mannose-Binding Lectin
0
Mbl2 protein, mouse
0
mannose binding protein A
143107-68-0
Complement C4b
80295-50-7
MASP-1 protein, mouse
EC 3.4.21.-
MASP-2 protein, mouse
EC 3.4.21.-
Mannose-Binding Protein-Associated Serine Proteases
EC 3.4.21.-
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
174Subventions
Organisme : Medical Research Council
ID : G0700859
Pays : United Kingdom
Organisme : Medical Research Council
ID : G1000191
Pays : United Kingdom
Organisme : Medical Research Council (MRC)
ID : MR/R002983/1
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