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Single cocaine exposure does not alter striatal pre‐synaptic dopamine function in mice: an [18F]‐FDOPA PET study 下载免费PDF全文
David R Bonsall Michelle Kokkinou Mattia Veronese Christopher Coello Lisa A. Wells Oliver D. Howes 《Journal of neurochemistry》2017,143(5):551-560
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Caveolin‐1 mediates tissue plasminogen activator‐induced MMP‐9 up‐regulation in cultured brain microvascular endothelial cells 下载免费PDF全文
Thrombolysis with tissue plasminogen activator (tPA) increases matrix metalloproteinase‐9 (MMP‐9) activity in the ischemic brain, which exacerbates blood‐brain barrier injury and increases the risk of symptomatic cerebral hemorrhage. The mechanism through which tPA enhances MMP‐9 activity is not well understood. Here we report an important role of caveolin‐1 in mediating tPA‐induced MMP‐9 synthesis. Brain microvascular endothelial cell line bEnd3 cells were incubated with 5 or 20 μg/ml tPA for 24 hrs before analyzing MMP‐9 levels in the conditioned media and cellular extracts by gelatin zymography. tPA at a dose of 20 μg/mL tPA, but not 5 μg/mL, significantly increased MMP‐9 level in cultured media while decreasing it in cellular extracts. Concurrently, tPA treatment induced a 2.3‐fold increase of caveolin‐1 protein levels in endothelial cells. Interestingly, knockdown of Cav‐1 with siRNA inhibited tPA‐induced MMP‐9 mRNA up‐regulation and MMP‐9 increase in the conditioned media, but did not affect MMP‐9 decrease in cellular extracts. These results suggest that caveolin‐1 critically contributes to tPA‐mediated MMP‐9 up‐regulation, but may not facilitate MMP‐9 secretion in endothelial cells.
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《Journal of neurochemistry》2014,130(4):467-468
- Did you know Journal of Neurochemistry offers authors the option to publish Open Access ? ISN members receive a reduced fee ($1,000 USD compared to the regular fee of $3,000 USD, less than most other journals charge).
- Download the new JNeurochem App for free: https:// itunes.apple.com/us/app/journal-neurochemistry-for/id655612235
- A virtual issue on Neuroinflammation in nervous system disorders, edited by Tammy Kielian, is now available: http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1471-4159/homepage/virtual_issues.htm#neuroinflammation
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Chemical hypoxia‐induced integrated stress response activation in oligodendrocytes is mediated by the transcription factor nuclear factor (erythroid‐derived 2)‐like 2 (NRF2) 下载免费PDF全文
Nico Teske Annette Liessem Felix Fischbach Tim Clarner Cordian Beyer Christoph Wruck Athanassios Fragoulis Simone C. Tauber Markus Kipp 《Journal of neurochemistry》2018,144(3):285-301
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Xueping Chen Wenyan Li Qiyan Cai Jianqin Niu Lan Xiao Jiming Kong 《Journal of neurochemistry》2013,127(3):426-433
Developing oligodendrocytes, collectively termed ‘pre‐myelinating oligodendrocytes’ (preOLs), are vulnerable to hypoxic or ischemic insults. The underlying mechanism of this vulnerability remains unclear. Previously, we showed that Bcl‐2?E1B‐19K‐interacting protein 3 (BNIP3), a proapoptotic member of the Bcl‐2 family proteins, induced neuronal death in a caspase‐independent manner in stroke. In this study, we investigated the role of BNIP3 in preOL cell death induced by hypoxia or ischemia. In primary oligodendrocyte progenitor cell (OPC) cultures exposed to oxygen–glucose deprivation, we found that BNIP3 was upregulated and levels of BNIP3 expression correlated with the death of OPCs. Up‐regulation of BNIP3 was observed in preOLs in the white matter in a neonatal rat model of stroke. Knockout of BNIP3 significantly reduced death of preOLs in the middle cerebral artery occlusion model in mice. Our results demonstrate a role of BNIP3 in mediating preOLs cell death induced by hypoxia or ischemia, and suggest that BNIP3 may be a new target for protecting oligodendrocytes from death after stroke.
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Adropin preserves the blood‐brain barrier through a Notch1/Hes1 pathway after intracerebral hemorrhage in mice 下载免费PDF全文
Lingyan Yu Zhengyang Lu Sherrefa Burchell Derek Nowrangi Anatol Manaenko Xue Li Yang Xu Ningbo Xu Jiping Tang Haibin Dai John H. Zhang 《Journal of neurochemistry》2017,143(6):750-760
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Reduced blood‐brain barrier expression of fatty acid‐binding protein 5 is associated with increased vulnerability of APP/PS1 mice to cognitive deficits from low omega‐3 fatty acid diets 下载免费PDF全文
Yijun Pan Kwok H. C. Choy Philip J. Marriott Siew Y. Chai Martin J. Scanlon Christopher J. H. Porter Jennifer L. Short Joseph A. Nicolazzo 《Journal of neurochemistry》2018,144(1):81-92
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Veronica Murta Priscila Schilrreff Gerardo Rosciszewski Maria Jose Morilla Alberto Javier Ramos 《Journal of neurochemistry》2018,144(6):748-760
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Vesicular GABA transporter (VGAT) is expressed in GABAergic and glycinergic neurons, and is responsible for vesicular storage and subsequent exocytosis of these inhibitory amino acids. In this study, we show that VGAT recognizes β‐alanine as a substrate. Proteoliposomes containing purified VGAT transport β‐alanine using Δψ but not ΔpH as a driving force. The Δψ‐driven β‐alanine uptake requires Cl?. VGAT also facilitates Cl? uptake in the presence of β‐alanine. A previously described VGAT mutant (Glu213Ala) that disrupts GABA and glycine transport similarly abrogates β‐alanine uptake. These findings indicated that VGAT transports β‐alanine through a mechanism similar to those for GABA and glycine, and functions as a vesicular β‐alanine transporter.
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《Journal of neurochemistry》2019,149(5):559-561
We are very sad that the ISN lost its President Kazuhiro Ikenaka, Professor and Chairman at National Institute for Physiological Sciences (NIPS), Director of Okazaki Institute of Integrative Biology. JNeurochem published an Obituary to value his outstanding achievements: Akio Wanaka et al. (2019) OBITUARY Kazuhiro Ikenaka (1952‐2018). https://doi.org/10.1111/jnc.14679
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Wnt signaling loss accelerates the appearance of neuropathological hallmarks of Alzheimer's disease in J20‐APP transgenic and wild‐type mice 下载免费PDF全文
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This editorial highlights a study by Rodriguez, Sanchez‐Moran et al. (2019) in the current issue of the Journal of Neurochemistry, in which the authors describe a microcephalic boy carrying the novel heterozygous de novo missense mutation c.560A> G; p.Asp187Gly in Cdh1/Fzr1 encoding the APC/C E3‐ubiquitin ligase cofactor CDH1. A functional characterization of mutant APC/CCDH1 confirms an aberrant division of neural progenitor cells, a condition known to determine the mouse brain cortex size. These data suggest that APC/CCDH1 may contribute to the regulation of the human brain size.
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Astrocytes with previous chronic exposure to amyloid β‐peptide fragment 1–40 suppress excitatory synaptic transmission 下载免费PDF全文
Hiroyuki Kawano Kohei Oyabu Hideaki Yamamoto Kei Eto Yuna Adaniya Kaori Kubota Takuya Watanabe Ayumi Hirano‐Iwata Junichi Nabekura Shutaro Katsurabayashi Katsunori Iwasaki 《Journal of neurochemistry》2017,143(6):624-634
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Liping Xu Chandrashekhar Voshavar Yevgeniya Shurubor Flint Beal Aloke K. Dutta 《Journal of neurochemistry》2014,131(1):74-85
In this study, in vitro and in vivo experiments were carried out with the high‐affinity multifunctional D2/D3 agonist D‐512 to explore its potential neuroprotective effects in models of Parkinson's disease and the potential mechanism(s) underlying such properties. Pre‐treatment with D‐512 in vitro was found to rescue rat adrenal Pheochromocytoma PC12 cells from toxicity induced by 6‐hydroxydopamine administration in a dose‐dependent manner. Neuroprotection was found to coincide with reductions in intracellular reactive oxygen species, lipid peroxidation, and DNA damage. In vivo, pre‐treatment with 0.5 mg/kg D‐512 was protective against neurodegenerative phenotypes associated with systemic administration of MPTP, including losses in striatal dopamine, reductions in numbers of DAergic neurons in the substantia nigra (SN), and locomotor dysfunction. These observations strongly suggest that the multifunctional drug D‐512 may constitute a novel viable therapy for Parkinson's disease.
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Cocaine‐ and amphetamine‐regulated transcript peptide in the nucleus accumbens shell inhibits cocaine‐induced locomotor sensitization to transient over‐expression of α‐Ca2+/calmodulin‐dependent protein kinase II 下载免费PDF全文
Lixia Xiong Qing Meng Xi Sun Xiangtong Lu Qiang Fu Qinghua Peng Jianhua Yang Ki‐Wan Oh Zhenzhen Hu 《Journal of neurochemistry》2018,146(3):289-303
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The role of glutamate signaling in incentive salience: second‐by‐second glutamate recordings in awake Sprague‐Dawley rats 下载免费PDF全文
Seth R. Batten Francois Pomerleau Jorge Quintero Greg A. Gerhardt Joshua S. Beckmann 《Journal of neurochemistry》2018,145(4):276-286
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Calmodulin‐like skin protein protects against spatial learning impairment in a mouse model of Alzheimer disease 下载免费PDF全文
Shinya Kusakari Mikiro Nawa Katsuko Sudo Masaaki Matsuoka 《Journal of neurochemistry》2018,144(2):218-233
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Janani Prahlad David N. Hauser Nicole M. Milkovic Mark R. Cookson Mark A. Wilson 《Journal of neurochemistry》2014,130(6):839-853
The oxidation of a key cysteine residue (Cys106) in the parkinsonism‐associated protein DJ‐1 regulates its ability to protect against oxidative stress and mitochondrial damage. Cys106 interacts with a neighboring protonated Glu18 residue, stabilizing the Cys106‐SO2? (sulfinic acid) form of DJ‐1. To study this important post‐translational modification, we previously designed several Glu18 mutations (E18N, E18D, E18Q) that alter the oxidative propensity of Cys106. However, recent results suggest these Glu18 mutations cause loss of DJ‐1 dimerization, which would severely compromise the protein's function. The purpose of this study was to conclusively determine the oligomerization state of these mutants using X‐ray crystallography, NMR spectroscopy, thermal stability analysis, circular dichroism spectroscopy, sedimentation equilibrium ultracentrifugation, and cross‐linking. We found that all of the Glu18 DJ‐1 mutants were dimeric. Thiol cross‐linking indicates that these mutant dimers are more flexible than the wild‐type protein and can form multiple cross‐linked dimeric species due to the transient exposure of cysteine residues that are inaccessible in the wild‐type protein. The enhanced flexibility of Glu18 DJ‐1 mutants provides a parsimonious explanation for their lower observed cross‐linking efficiency in cells. In addition, thiol cross‐linkers may have an underappreciated value as qualitative probes of protein conformational flexibility.