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

Nakano, Yusuke; Suzuki, Yukiya; Takagi, Toshinori; Kitashoji, Akira; Ono, Yoko; Tsuruma, Kazuhiro; Yoshimura, Shinichi; Shimazawa, Masamitsu; Iwama, Toru; Hara, Hideaki

doi:10.1016/j.neuroscience.2014.06.065

Cited by 47 publications

(45 citation statements)

References 31 publications

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“…Analysis of function in GeneCards revealed that EPHB1 and UNC5B also regulate angiogenesis (Safran et al, 2010). Literature reports that ANGPTL4 upregulation corresponds to increased vascularization after stroke (Schipper et al, 2014). Results from prior studies show that IL21R, BMF , and GPNMB correspond to mediators of injury following ischemic stroke (Clarkson et al, 2014; Nakano et al, 2014; Pfeiffer et al, 2014).…”

Section: Resultsmentioning

confidence: 99%

Hydrogel scaffolds promote neural gene expression and structural reorganization in human astrocyte cultures

Knight

Serrano

2017

PeerJ

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Biomaterial scaffolds have the potential to enhance neuronal development and regeneration. Understanding the genetic responses of astrocytes and neurons to biomaterials could facilitate the development of synthetic environments that enable the specification of neural tissue organization with engineered scaffolds. In this study, we used high throughput transcriptomic and imaging methods to determine the impact of a hydrogel, PuraMatrix™, on human glial cells in vitro. Parallel studies were undertaken with cells grown in a monolayer environment on tissue culture polystyrene. When the Normal Human Astrocyte (NHA) cell line is grown in a hydrogel matrix environment, the glial cells adopt a structural organization that resembles that of neuronal-glial cocultures, where neurons form clusters that are distinct from the surrounding glia. Statistical analysis of next generation RNA sequencing data uncovered a set of genes that are differentially expressed in the monolayer and matrix hydrogel environments. Functional analysis demonstrated that hydrogel-upregulated genes can be grouped into three broad categories: neuronal differentiation and/or neural plasticity, response to neural insult, and sensory perception. Our results demonstrate that hydrogel biomaterials have the potential to transform human glial cell identity, and may have applications in the repair of damaged brain tissue.

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Section: Resultsmentioning

confidence: 99%

Hydrogel scaffolds promote neural gene expression and structural reorganization in human astrocyte cultures

Knight

Serrano

2017

PeerJ

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“…GPNMB is increased in skeletal muscle in a mouse model of denervation and protects against muscular atrophy (Furochi et al, ; Ogawa et al, ). GPNMB improves memory and shows a protective effect against cerebral ischemia‐reperfusion injury (Murata et al, ; Nakano et al, ).…”

Section: Introductionmentioning

confidence: 99%

GPNMB ameliorates mutant TDP‐43‐induced motor neuron cell death

Nagahara

Shimazawa

Ohuchi

et al. 2016

J of Neuroscience Research

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Glycoprotein nonmetastatic melanoma protein B (GPNMB) aggregates are observed in the spinal cord of amyotrophic lateral sclerosis (ALS) patients, but the detailed localization is still unclear. Mutations of transactive response DNA binding protein 43kDa (TDP-43) are associated with neurodegenerative diseases including ALS. In this study, we evaluated the localization of GPNMB aggregates in the spinal cord of ALS patients and the effect of GPNMB against mutant TDP-43 induced motor neuron cell death. GPNMB aggregates were not localized in the glial fibrillary acidic protein (GFAP)-positive astrocyte and ionized calcium binding adaptor molecule-1 (Iba1)-positive microglia. GPNMB aggregates were localized in the microtubule-associated protein 2 (MAP-2)-positive neuron and neurofilament H non-phosphorylated (SMI-32)-positive neuron, and these were co-localized with TDP-43 aggregates in the spinal cord of ALS patients. Mock or TDP-43 (WT, M337V, and A315T) plasmids were transfected into mouse motor neuron cells (NSC34). The expression level of GPNMB was increased by transfection of mutant TDP-43 plasmids. Recombinant GPNMB ameliorated motor neuron cell death induced by transfection of mutant TDP-43 plasmids and serum-free stress. Furthermore, the expression of phosphorylated ERK1/2 and phosphorylated Akt were decreased by this stress, and these expressions were increased by recombinant GPNMB. These results indicate that GPNMB has protective effects against mutant TDP-43 stress via activating the ERK1/2 and Akt pathways, and GPNMB may be a therapeutic target for TDP-43 proteinopathy in familial and sporadic ALS. © 2016 Wiley Periodicals, Inc.

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“…GPNMB plays a role in extracellular matrix (ECM) remodeling in osteoblast and fibroblast differentiation and in increasing cancer metastasis by induction of matrix metalloproteinases (MMP)3 and MMP9 (3,(7)(8)(9)(10). Importantly, GPNMB promotes regeneration after muscle, kidney, liver, and cerebral ischemiareperfusion injury by regulation of immune/inflammatory responses and suppressing fibrosis (11)(12)(13)(14). However, the functions of GPNMB in pathophysiological processes in the heart are still unknown, although GPNMB was recently mentioned in a screen of viral cardiomyopathy (15).…”

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confidence: 99%

Adverse left ventricular remodeling by glycoprotein nonmetastatic melanoma protein B in myocardial infarction

et al. 2016

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Cardiac diseases are the leading cause of death. Available treatment approaches are not sufficient to reverse persistent cardiac damage after injury; thus, the search for new therapeutic targets is essential. Our microarray-based screening in rat hearts 24 h after myocardial infarction (MI) yielded glycoprotein nonmetastatic melanoma protein B (GPNMB), which is known to be involved in inflammation and fibrosis after tissue injury. However, its role in the heart was elusive. We found increased cardiac expression levels of GPNMB in rats and mice after MI. Analysis of DBA/2J mice, which lack functional GPNMB due to a spontaneous point mutation, showed that systemic GPNMB deficiency was associated with preserved cardiac function and less left ventricular dilation after MI compared with DBA/2J mice with reconstituted GPNMB expression. These improvements were associated with decreased expression of matrix metalloproteinase 9, the cardiac stress genes for natriuretic peptides (atrial natriuretic peptide and brain natriuretic peptide), and β-myosin heavy chain after MI. Moreover, GPNMB deficiency attenuated the dilated cardiomyopathy in muscle lim protein knockout mice but could not prevent cardiac hypertrophy induced by isoprenaline infusion. This is the first experimental study to show that GPNMB adversely influences myocardial remodeling.-Järve, A., Mühlstedt, S., Qadri, F., Nickl, B., Schulz, H., Hübner, N., Özcelik, C., Bader, M. Adverse left ventricular remodeling by glycoprotein nonmetastatic melanoma protein B in myocardial infarction.

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

Cited by 47 publications

References 31 publications

Hydrogel scaffolds promote neural gene expression and structural reorganization in human astrocyte cultures

Hydrogel scaffolds promote neural gene expression and structural reorganization in human astrocyte cultures

GPNMB ameliorates mutant TDP‐43‐induced motor neuron cell death

Adverse left ventricular remodeling by glycoprotein nonmetastatic melanoma protein B in myocardial infarction

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