cRel and Wnt5a/Frizzled 5 Receptor-Mediated Inflammatory Regulation Reveal Novel Neuroprotectin D1 Targets for Neuroprotection.

Human RPE cells Inflammatory cytokines Ischemia–reperfusion Neuroprotectin D1 Neuroprotection Non-conventional cytokine Retinal pigment epithelial cells Stroke Uncompensated oxidative stress Wnt5a promoter

Journal

Cellular and molecular neurobiology
ISSN: 1573-6830
Titre abrégé: Cell Mol Neurobiol
Pays: United States
ID NLM: 8200709

Informations de publication

Date de publication:
Apr 2023
Historique:
received: 14 04 2022
accepted: 10 05 2022
pubmed: 28 5 2022
medline: 15 3 2023
entrez: 27 5 2022
Statut: ppublish

Résumé

Wnt5a triggers inflammatory responses and damage via NFkB/p65 in retinal pigment epithelial (RPE) cells undergoing uncompensated oxidative stress (UOS) and in experimental ischemic stroke. We found that Wnt5a-Clathrin-mediated uptake leads to NFkB/p65 activation and that Wnt5a is secreted in an exosome-independent fashion. We uncovered that docosahexaenoic acid (DHA) and its derivative, Neuroprotectin D1 (NPD1), upregulate c-Rel expression that, as a result, blunts Wnt5a abundance by competing with NFkB/p65 on the Wnt5a promoter A. Wnt5a increases in ischemic stroke penumbra and blood, while DHA reduces Wnt5a abundance with concomitant neuroprotection. Peptide inhibitor of Wnt5a binding, Box5, is also neuroprotective. DHA-decreased Wnt5a expression is concurrent with a drop in NFkB-driven inflammatory cytokine expression, revealing mechanisms after stroke, as in RPE cells exposed to UOS. Limiting the Wnt5a activity via Box5 reduces stroke size, suggesting neuroprotection pertinent to onset and progression of retinal degenerations and stroke consequences. NPD1 disrupts Wnt5a feedback loop at two sites: (1) decreasing FZD5, thus Wnt5a internalization, and (2) by enhancing cREL activity, which competes with p65/NFkB downstream endocytosis. As a result, Wnt5a expression is reduced, and so is its inflammatory signaling in RPE cells and neurons in ischemic stroke.

Identifiants

pubmed: 35622188
doi: 10.1007/s10571-022-01231-6
pii: 10.1007/s10571-022-01231-6
pmc: PMC10006067
doi:

Substances chimiques

Docosahexaenoic Acids 25167-62-8
protectin D1 0
Wnt-5a Protein 0
WNT5A protein, human 0
Frizzled Receptors 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1077-1096

Subventions

Organisme : NEI NIH HHS
ID : R01 EY005121
Pays : United States
Organisme : NEI NIH HHS
ID : R01EY005121
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS104117
Pays : United States
Organisme : NINDS NIH HHS
ID : R01NS104117
Pays : United States
Organisme : NINDS NIH HHS
ID : R01NS104117
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS109221
Pays : United States
Organisme : NEI NIH HHS
ID : R01EY005121
Pays : United States

Commentaires et corrections

Type : ErratumIn

Informations de copyright

© 2022. The Author(s).

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Auteurs

Jorgelina M Calandria (JM)

Neuroscience Center of Excellence, School of Medicine, Louisiana State University Health New Orleans, New Orleans, LA, 70112, USA.

Khanh V Do (KV)

Neuroscience Center of Excellence, School of Medicine, Louisiana State University Health New Orleans, New Orleans, LA, 70112, USA.
Faculty of Medicine, PHENIKAA University, and PHENIKAA Research and Technology Institute (PRATI), A&A Green Phoenix Group JSC, Hanoi, Vietnam.

Sayantani Kala-Bhattacharjee (S)

Neuroscience Center of Excellence, School of Medicine, Louisiana State University Health New Orleans, New Orleans, LA, 70112, USA.

Andre Obenaus (A)

Department of Pediatrics, University of California, Irvine, CA, 92618, USA.

Ludmila Belayev (L)

Neuroscience Center of Excellence, School of Medicine, Louisiana State University Health New Orleans, New Orleans, LA, 70112, USA.

Nicolas G Bazan (NG)

Neuroscience Center of Excellence, School of Medicine, Louisiana State University Health New Orleans, New Orleans, LA, 70112, USA. nbazan@lsuhsc.edu.

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Classifications MeSH