Glycoprotein nonmetastatic melanoma protein B (GPNMB) as a novel neuroprotective factor in cerebral ischemia–reperfusion injury

Highlights • GPNMB expression is up-regulated after ischemia–reperfusion injury. • GPNMB significantly ameliorated infarct volume. • The protective mechanism of GPNMB will be involvement of phosphorylation of ERK1/2 and Akt.

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Bibliographic Details
Published in:Neuroscience 2014-09, Vol.277, p.123-131
Main Authors: Nakano, Y, Suzuki, Y, Takagi, T, Kitashoji, A, Ono, Y, Tsuruma, K, Yoshimura, S, Shimazawa, M, Iwama, T, Hara, H
Format: Article
Language:English
Subjects:
Adult
Aged
Animals
Astrocytes - metabolism
Astrocytes - pathology
Brain - metabolism
Brain - pathology
Brain Ischemia - metabolism
Brain Ischemia - pathology
Disease Models, Animal
Epilepsy - metabolism
extracellular Signal-regulated kinase 1 and 2 (ERK)
Extracellular Space - metabolism
Eye Proteins - genetics
Eye Proteins - metabolism
Female
glycoprotein nonmetastatic melanoma protein B (GPNMB)
Humans
Infarction, Middle Cerebral Artery
Male
MAP Kinase Signaling System - physiology
Membrane Glycoproteins - genetics
Membrane Glycoproteins - metabolism
Mice
Mice, Transgenic
Neurology
Neurons - metabolism
Neurons - pathology
neuroprotection
protein kinase B (Akt)
Proto-Oncogene Proteins c-akt - metabolism
Recombinant Proteins - genetics
Recombinant Proteins - metabolism
Reperfusion Injury - metabolism
Reperfusion Injury - pathology
stroke
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Description
Summary:Highlights • GPNMB expression is up-regulated after ischemia–reperfusion injury. • GPNMB significantly ameliorated infarct volume. • The protective mechanism of GPNMB will be involvement of phosphorylation of ERK1/2 and Akt.
ISSN:0306-4522
1873-7544
DOI:10.1016/j.neuroscience.2014.06.065