Disruption of Midkine gene reduces traumatic brain injury through the modulation of neuroinflammation.
Animals
Apoptosis
/ genetics
Astrocytes
/ pathology
Brain
/ pathology
Brain Injuries, Traumatic
/ genetics
Calcium-Binding Proteins
/ metabolism
Cell Polarity
/ genetics
Encephalitis
/ genetics
Glial Fibrillary Acidic Protein
/ metabolism
Mice
Mice, Inbred C57BL
Mice, Knockout
Microfilament Proteins
/ metabolism
Microglia
/ pathology
Midkine
/ genetics
RNA, Messenger
/ biosynthesis
M1/M2 phenotype
Microglia/macrophages
Midkine
Neuroinflammation
Traumatic brain injury
Journal
Journal of neuroinflammation
ISSN: 1742-2094
Titre abrégé: J Neuroinflammation
Pays: England
ID NLM: 101222974
Informations de publication
Date de publication:
29 Jan 2020
29 Jan 2020
Historique:
received:
17
08
2019
accepted:
12
01
2020
entrez:
31
1
2020
pubmed:
31
1
2020
medline:
13
11
2020
Statut:
epublish
Résumé
Midkine (MK) is a multifunctional cytokine found upregulated in the brain in the presence of different disorders characterized by neuroinflammation, including neurodegenerative disorders and ischemia. The neuroinflammatory response to traumatic brain injury (TBI) represents a key secondary injury factor that can result in further neuronal injury. In the present study, we investigated the role of endogenous MK in secondary injury, including neuroinflammation, immune response, and neuronal apoptosis activity, after TBI. Wild type (Mdk As opposed to Mdk Our findings suggest that MK-deficiency reduced tissue infiltration of microglia/macrophages and altered their polarization status thereby reducing neuroinflammation, neuronal apoptosis, and tissue loss and improving neurological outcomes after TBI. Therefore, targeting MK to modulate neuroinflammation may represent a potential therapeutic strategy for TBI management.
Sections du résumé
BACKGROUND
BACKGROUND
Midkine (MK) is a multifunctional cytokine found upregulated in the brain in the presence of different disorders characterized by neuroinflammation, including neurodegenerative disorders and ischemia. The neuroinflammatory response to traumatic brain injury (TBI) represents a key secondary injury factor that can result in further neuronal injury. In the present study, we investigated the role of endogenous MK in secondary injury, including neuroinflammation, immune response, and neuronal apoptosis activity, after TBI.
METHODS
METHODS
Wild type (Mdk
RESULTS
RESULTS
As opposed to Mdk
CONCLUSION
CONCLUSIONS
Our findings suggest that MK-deficiency reduced tissue infiltration of microglia/macrophages and altered their polarization status thereby reducing neuroinflammation, neuronal apoptosis, and tissue loss and improving neurological outcomes after TBI. Therefore, targeting MK to modulate neuroinflammation may represent a potential therapeutic strategy for TBI management.
Identifiants
pubmed: 31996236
doi: 10.1186/s12974-020-1709-8
pii: 10.1186/s12974-020-1709-8
pmc: PMC6990546
doi:
Substances chimiques
Aif1 protein, mouse
0
Calcium-Binding Proteins
0
Glial Fibrillary Acidic Protein
0
Mdk protein, mouse
0
Microfilament Proteins
0
RNA, Messenger
0
glial fibrillary astrocytic protein, mouse
0
Midkine
137497-38-2
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
40Références
J Neurosci. 2009 Oct 28;29(43):13435-44
pubmed: 19864556
Neurosci Lett. 2018 Jan 1;662:213-218
pubmed: 29061398
Proc Natl Acad Sci U S A. 2008 Mar 11;105(10):3915-20
pubmed: 18319343
Brain Res Bull. 2018 Jun;140:154-161
pubmed: 29698747
J Neurosci. 1995 Dec;15(12):8223-33
pubmed: 8613756
Nat Commun. 2017 Jun 01;8:15080
pubmed: 28569747
J Immunol. 2001 Sep 15;167(6):3463-9
pubmed: 11544339
Cancer Res. 1993 Mar 15;53(6):1281-5
pubmed: 8383007
J Immunol. 2012 Mar 15;188(6):2602-11
pubmed: 22323540
Neural Regen Res. 2014 Oct 15;9(20):1787-95
pubmed: 25422640
J Neuroinflammation. 2017 Aug 23;14(1):167
pubmed: 28835272
EBioMedicine. 2019 Mar;41:185-199
pubmed: 30773478
Neurotherapeutics. 2010 Jan;7(1):3-12
pubmed: 20129492
Biochem Biophys Res Commun. 1993 Apr 15;192(1):246-51
pubmed: 8476427
Immunol Cell Biol. 2011 Jan;89(1):130-42
pubmed: 20514074
Curr Pharm Des. 2011;17(5):410-23
pubmed: 21375488
Proc Jpn Acad Ser B Phys Biol Sci. 2010;86(4):410-25
pubmed: 20431264
Arthritis Rheum. 2004 May;50(5):1420-9
pubmed: 15146411
Mod Rheumatol. 2019 Jul;29(4):567-571
pubmed: 30217121
Cereb Cortex. 2013 Jul;23(7):1742-55
pubmed: 22700645
Neurosci Lett. 2013 Aug 29;550:150-5
pubmed: 23811026
J Biochem. 2013 Jun;153(6):511-21
pubmed: 23625998
Mediators Inflamm. 2016;2016:9894504
pubmed: 28044069
J Neuroinflammation. 2016 Oct 11;13(1):264
pubmed: 27724914
Acta Histochem. 2014 Mar;116(2):319-26
pubmed: 24055194
Neurotherapeutics. 2010 Oct;7(4):366-77
pubmed: 20880501
Stroke. 2012 Nov;43(11):3063-70
pubmed: 22933588
J Clin Invest. 2000 Feb;105(4):489-95
pubmed: 10683378
Liver Int. 2004 Oct;24(5):484-91
pubmed: 15482347
Lancet. 2000 Sep 9;356(9233):923-9
pubmed: 11036909
J Neuroinflammation. 2014 Apr 24;11:82
pubmed: 24761998
J Neurotrauma. 2004 Apr;21(4):471-7
pubmed: 15115596
J Am Coll Surg. 2005 Sep;201(3):343-8
pubmed: 16125066
J Cereb Blood Flow Metab. 2013 Dec;33(12):1864-74
pubmed: 23942366
Front Pharmacol. 2019 Apr 12;10:377
pubmed: 31031625
J Neurosci Res. 2009 Oct;87(13):2908-15
pubmed: 19437545
Exp Neurol. 2016 Jan;275 Pt 3:316-327
pubmed: 26342753
Front Neurol. 2019 May 22;10:509
pubmed: 31178814
J Head Trauma Rehabil. 2008 Mar-Apr;23(2):123-31
pubmed: 18362766
Br J Pharmacol. 2016 Feb;173(4):692-702
pubmed: 25752446
J Neuroinflammation. 2011 Jul 06;8:78
pubmed: 21733162
J Cereb Blood Flow Metab. 2017 Mar;37(3):967-979
pubmed: 27174997
Blood. 2014 Mar 20;123(12):1887-96
pubmed: 24458438
Eur J Immunol. 2015 Jan;45(1):180-91
pubmed: 25329858
Stroke. 1998 Oct;29(10):2136-40
pubmed: 9756595
Brain Res Dev Brain Res. 1995 Mar 16;85(1):25-30
pubmed: 7781164