Transient Receptor Potential Vanilloid 4-Dependent Microglial Function in Myelin Injury and Repair.
EAE
TRPV4
cuprizone
disease activity
experimental autoimmune encephalitis
inflammation
microglia
multiple sclerosis
transient receptor potential vanilloid 4
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
04 Dec 2023
04 Dec 2023
Historique:
received:
18
09
2023
revised:
01
11
2023
accepted:
21
11
2023
medline:
9
12
2023
pubmed:
9
12
2023
entrez:
9
12
2023
Statut:
epublish
Résumé
Microglia are found pathologically at all stages of multiple sclerosis (MS) lesion development and are hypothesized to contribute to both inflammatory injury and neuroprotection in the MS brain. Transient receptor potential vanilloid 4 (TRPV4) channels are widely expressed, play an important role as environmental sensors, and are involved in calcium homeostasis for a variety of cells. TRPV4 modulates myeloid cell phagocytosis in the periphery and microglial motility in the central nervous system. We hypothesized that TRPV4 deletion would alter microglia phagocytosis in vitro and lessen disease activity and demyelination in experimental autoimmune encephalitis (EAE) and cuprizone-induced demyelination. We found that genetic deletion of TRPV4 led to increased microglial phagocytosis in vitro but did not alter the degree of demyelination or remyelination in the cuprizone mouse model of MS. We also found no difference in disease in EAE following global or microglia-specific deletion of
Identifiants
pubmed: 38069420
pii: ijms242317097
doi: 10.3390/ijms242317097
pmc: PMC10706888
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NINDS NIH HHS
ID : R01NS106289
Pays : United States
Organisme : NINDS NIH HHS
ID : R25NS090978
Pays : United States
Références
J Neuroimmunol. 2010 Jun;223(1-2):39-54
pubmed: 20451260
Acta Neuropathol. 2017 Jan;133(1):25-42
pubmed: 27796537
Brain. 2009 May;132(Pt 5):1175-89
pubmed: 19339255
Front Cell Dev Biol. 2020 Aug 27;8:849
pubmed: 32974355
Brain. 2017 Jul 1;140(7):1900-1913
pubmed: 28541408
Mult Scler. 2020 Dec;26(14):1816-1821
pubmed: 33174475
Brain. 2009 Feb;132(Pt 2):288-95
pubmed: 18567623
J Physiol. 2005 Aug 15;567(Pt 1):53-8
pubmed: 15961428
Neurosci Lett. 2009 Apr 3;453(2):120-5
pubmed: 19356606
Cell J. 2017 Apr-Jun;19(1):1-10
pubmed: 28367411
J Neuropathol Exp Neurol. 2015 Jan;74(1):48-63
pubmed: 25470347
Physiol Rev. 2016 Jul;96(3):911-73
pubmed: 27252279
Am J Pathol. 1990 Sep;137(3):575-84
pubmed: 1698025
Exp Physiol. 2016 Dec 1;101(12):1472-1476
pubmed: 27701788
Front Neurol. 2019 Jan 29;10:30
pubmed: 30761069
Int J Mol Sci. 2019 Jan 03;20(1):
pubmed: 30609838
Acta Neuropathol. 2013 Apr;125(4):595-608
pubmed: 23354834
Glia. 2012 May;60(5):761-70
pubmed: 22331560
J Autoimmun. 2011 Feb;36(1):56-64
pubmed: 21095100
J Biol Chem. 2003 Jun 20;278(25):22664-8
pubmed: 12692122
J Immunol. 2016 Jan 1;196(1):428-36
pubmed: 26597012
J Exp Med. 2004 Jul 5;200(1):79-87
pubmed: 15238607
J Allergy Clin Immunol. 2018 Feb;141(2):608-619.e7
pubmed: 28807414
Adv Pharmacol. 2017;79:117-139
pubmed: 28528666
Glia. 2022 Nov;70(11):2157-2168
pubmed: 35809029
J Exp Med. 2015 Apr 6;212(4):481-95
pubmed: 25779633
Cell Death Dis. 2019 May 16;10(6):386
pubmed: 31097691
Neurosci Res. 2012 Jan;72(1):32-42
pubmed: 22015947
Proc Natl Acad Sci U S A. 2012 Jan 17;109(3):965-70
pubmed: 22219359
Bio Protoc. 2016 Nov 5;6(21):
pubmed: 29104890
Glia. 2021 Jun;69(6):1563-1582
pubmed: 33624376
Nat Rev Neurosci. 2014 May;15(5):300-12
pubmed: 24713688
ASN Neuro. 2014 Sep 30;6(5):
pubmed: 25290063
J Clin Invest. 2023 Mar 1;133(5):
pubmed: 36701202
Brain Behav Immun. 2010 May;24(4):641-51
pubmed: 20138983
Front Cell Neurosci. 2018 Nov 05;12:392
pubmed: 30455633
Cell Immunol. 1991 May;134(2):505-10
pubmed: 1902401