EPO regulates neuroprotective Transmembrane BAX Inhibitor-1 Motif-containing (TMBIM) family members GRINA and FAIM2 after cerebral ischemia-reperfusion injury.


Journal

Experimental neurology
ISSN: 1090-2430
Titre abrégé: Exp Neurol
Pays: United States
ID NLM: 0370712

Informations de publication

Date de publication:
10 2019
Historique:
received: 02 05 2019
revised: 03 06 2019
accepted: 12 06 2019
pubmed: 19 6 2019
medline: 4 3 2020
entrez: 19 6 2019
Statut: ppublish

Résumé

Transmembrane BAX Inhibitor-1 Motif-containing (TMBIM) family members exert inhibitory activities in apoptosis and necroptosis. FAIM2 (TMBIM-2) is neuroprotective against murine focal ischemia and is regulated by erythropoietin (EPO). Similar to FAIM2, GRINA (TMBIM-3) is predominantly expressed in the brain. The role of GRINA in transient brain ischemia, its potential synergistic effects with FAIM2 and its regulation by EPO treatment were assessed. We performed transient (30 min) middle cerebral artery occlusion (tMCAo) followed by 72 h of reperfusion in GRINA-deficient (GRINA Compared to wildtype controls GRINA deficiency led to a similar increase in infarct volumes as FAIM2 deficiency (p < .01). We observed the highest neurological deficits and largest infarct sizes in double-deficient mice. EPO administration upregulated GRINA and FAIM2 mRNA levels in wildtype littermates. EPO decreased infarct sizes and abrogated neurological impairments in wildtype controls. GRINA and/or FAIM2 deficient mice showed increased expression levels of cleaved-caspase 3 and of pro-apoptotic BAX mRNA. Further, caspase 8 was upregulated in FAIM2 GRINA and FAIM2 are highly expressed in the brain and convey EPO-mediated neuroprotection after ischemic stroke involving different caspases.

Sections du résumé

BACKGROUND AND PURPOSE
Transmembrane BAX Inhibitor-1 Motif-containing (TMBIM) family members exert inhibitory activities in apoptosis and necroptosis. FAIM2 (TMBIM-2) is neuroprotective against murine focal ischemia and is regulated by erythropoietin (EPO). Similar to FAIM2, GRINA (TMBIM-3) is predominantly expressed in the brain. The role of GRINA in transient brain ischemia, its potential synergistic effects with FAIM2 and its regulation by EPO treatment were assessed.
METHODS
We performed transient (30 min) middle cerebral artery occlusion (tMCAo) followed by 72 h of reperfusion in GRINA-deficient (GRINA
RESULTS
Compared to wildtype controls GRINA deficiency led to a similar increase in infarct volumes as FAIM2 deficiency (p < .01). We observed the highest neurological deficits and largest infarct sizes in double-deficient mice. EPO administration upregulated GRINA and FAIM2 mRNA levels in wildtype littermates. EPO decreased infarct sizes and abrogated neurological impairments in wildtype controls. GRINA and/or FAIM2 deficient mice showed increased expression levels of cleaved-caspase 3 and of pro-apoptotic BAX mRNA. Further, caspase 8 was upregulated in FAIM2
CONCLUSIONS
GRINA and FAIM2 are highly expressed in the brain and convey EPO-mediated neuroprotection after ischemic stroke involving different caspases.

Identifiants

pubmed: 31211943
pii: S0014-4886(19)30130-X
doi: 10.1016/j.expneurol.2019.112978
pii:
doi:

Substances chimiques

Epoetin Alfa 64FS3BFH5W
Grina protein, mouse 0
lifeguard protein, mouse 0
Membrane Proteins 0
Nerve Tissue Proteins 0
Neuroprotective Agents 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

112978

Informations de copyright

Copyright © 2019 Elsevier Inc. All rights reserved.

Auteurs

Pardes Habib (P)

Department of Neurology, Medical School, RWTH Aachen University, Aachen, Germany. Electronic address: phabib@ukaachen.de.

Ann-Sophie Stamm (AS)

Department of Neurology, Medical School, RWTH Aachen University, Aachen, Germany.

Thomas Zeyen (T)

Department of Neurology, Medical School, RWTH Aachen University, Aachen, Germany.

Rozina Noristani (R)

Department of Neurology, Medical School, RWTH Aachen University, Aachen, Germany.

Alexander Slowik (A)

Institute of Neuroanatomy, Medical School, RWTH Aachen University, Aachen, Germany.

Cordian Beyer (C)

Institute of Neuroanatomy, Medical School, RWTH Aachen University, Aachen, Germany.

Thomas Wilhelm (T)

Institute of Biochemistry and Molecular Immunology, Medical School, RWTH Aachen University, Aachen, Germany.

Michael Huber (M)

Institute of Biochemistry and Molecular Immunology, Medical School, RWTH Aachen University, Aachen, Germany.

Daniel Komnig (D)

Department of Neurology, Medical School, RWTH Aachen University, Aachen, Germany.

Jörg B Schulz (JB)

Department of Neurology, Medical School, RWTH Aachen University, Aachen, Germany; JARA-BRAIN Institute of Molecular Neuroscience and Neuroimaging, Forschungszentrum Jülich GmbH and RWTH Aachen University, Aachen, Germany.

Arno Reich (A)

Department of Neurology, Medical School, RWTH Aachen University, Aachen, Germany.

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Classifications MeSH