Journal of Neurochemistry

Cover image for Vol. 132 Issue 3

Edited By: Jörg Schulz

Impact Factor: 4.244

ISI Journal Citation Reports © Ranking: 2013: 63/252 (Neurosciences); 74/291 (Biochemistry & Molecular Biology)

Online ISSN: 1471-4159

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Recently Published Articles

  1. Heat shock protein responses to aging and proteotoxicity in the olfactory bulb

    Tyler S. Crum, Amanda M. Gleixner, Jessica M. Posimo, Daniel M. Mason, Matthew T. Broeren, Scott D. Heinemann, Peter Wipf, Jeffrey L. Brodsky and Rehana K. Leak

    Accepted manuscript online: 29 JAN 2015 09:17AM EST | DOI: 10.1111/jnc.13041

  2. Lipocalin-2 enhances angiogenesis in rat brain endothelial cells via reactive oxygen species and iron-dependent mechanisms

    Limin Wu, Yang Du, Josephine Lok, Eng H. Lo and Changhong Xing

    Article first published online: 29 JAN 2015 | DOI: 10.1111/jnc.13023

    Thumbnail image of graphical abstract

    Angiogenesis is an important part of stroke recovery. In the present study, we examined the hypothesis that lipocalin-2 (LCN2) may enhance angiogenesis in brain endothelial cells. LCN2 promoted tube formation and migration via iron and ROS-related pathways in rat brain endothelial cells. ROS scavengers, Nox inhibitors and iron chelators all dampened the ability of LCN2 to enhance in vitro angiogenesis. These findings support the idea that LCN2 that is released by damaged neurons may act as a ‘help me’ signal that promotes neurovascular recovery after stroke and brain injury.

  3. The extracellular fragment of GPNMB (Glycoprotein nonmelanosoma protein B, osteoactivin) improves memory and increases hippocampal GluA1 levels in mice

    Kenta Murata, Yuta Yoshino, Kazuhiro Tsuruma, Shigeki Moriguchi, Atsushi Oyagi, Hirotaka Tanaka, Mitsue Ishisaka, Masamitsu Shimazawa, Kohji Fukunaga and Hideaki Hara

    Article first published online: 29 JAN 2015 | DOI: 10.1111/jnc.13010

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    Glycoprotein nonmelanoma protein B (GPNMB) is widely expressed in neurons. We investigated the role of GPNMB on memory by using transgenic mice over-expressing GPNMB (Tg) and GPNMB extracellular fragment (ECF)-treated mice. Both mice exhibited memory improvement. In Tg mice, protein levels of phosphorylated α-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptor subunit GluA1, CaMK2 (Ca2+/calmodulin-dependent protein kinase 2), and GSK3β (glycogen synthase kinase 3β) were increased. Tg mice and ECF-treated hippocampus promoted LTP. These findings suggest that GPNMB might become a novel target for research on higher order brain functions.

  4. Rapid mitochondrial dysfunction mediates TNF-alpha-induced neurotoxicity

    Danielle N. Doll, Stephanie L. Rellick, Taura L. Barr, Xuefang Ren and James W. Simpkins

    Article first published online: 29 JAN 2015 | DOI: 10.1111/jnc.13008

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    This study focuses on the neurotoxic mechanism of a pro-inflammatory cytokine, tumor necrosis factor alpha (TNF-α). We demonstrate a prompt mitochondrial dysfunction followed by nerve cell loss after exposure to TNF-α. These studies may provide evidence that the immune system can rapidly and adversely affect brain function and that TNF-α signaling may be a target for neuroprotection.

  5. Sigma receptor 1 activation attenuates release of inflammatory cytokines MIP1γ, MIP2, MIP3α, and IL12 (p40/p70) by retinal Müller glial cells

    Arul Shanmugam, Jing Wang, Shanu Markand, Richard L. Perry, Amany Tawfik, Eric Zorrilla, Vadivel Ganapathy and Sylvia B. Smith

    Article first published online: 29 JAN 2015 | DOI: 10.1111/jnc.13002

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    A common feature of retinal disease is Müller cell reactive gliosis, which includes cytokine release. To understand how sigma receptor 1 (σR1) mediates neuroprotection, we examined the effects of a high-affinity σR1 ligand, (+)-pentazocine, on LPS-stimulated cytokine release in primary mouse retinal Müller glial cells. Under basal conditions, cytokine release was minimal. LPS stimulation markedly increased secretion of the cytokines MIP1γ, MIP2, MIP3α, IL12 (p40/p70), which was accompanied by a significant translocation of NFκB from cytoplasm to the nucleus. LPS-treatment in the presence of (+)-pentazocine markedly decreased cytokine release accompanied by a significant decrease in NFκB localized to the nucleus. IL, interleukin; MIP, macrophage inflammatory proteins.