共查询到20条相似文献,搜索用时 375 毫秒
1.
Screening the expression characteristics of several miRNAs in G93A‐SOD1 transgenic mouse: altered expression of miRNA‐124 is associated with astrocyte differentiation by targeting Sox2 and Sox9 下载免费PDF全文
Fenghua Zhou Caixia Zhang Yingjun Guan Yanchun Chen Qiang Lu Linlin Jie Hailing Gao Hongmei Du Haoyun Zhang Yongxin Liu Xin Wang 《Journal of neurochemistry》2018,145(1):51-67
2.
Hippocampal nuclear factor kappa B accounts for stress‐induced anxiety behaviors via enhancing neuronal nitric oxide synthase (nNOS)‐carboxy‐terminal PDZ ligand of nNOS‐Dexras1 coupling 下载免费PDF全文
Li‐Juan Zhu Huan‐Yu Ni Rong Chen Lei Chang Hu‐Jiang Shi Dan Qiu Zhan Zhang Dan‐Lian Wu Zhao‐Chun Jiang Hong‐Liang Xin Qi‐Gang Zhou Dong‐Ya Zhu 《Journal of neurochemistry》2018,146(5):598-612
3.
Cyclophilin D regulates neuronal activity‐induced filopodiagenesis by fine‐tuning dendritic mitochondrial calcium dynamics 下载免费PDF全文
Shaomei Sui Jing Tian Esha Gauba Qi Wang Lan Guo Heng Du 《Journal of neurochemistry》2018,146(4):403-415
4.
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
5.
The role of S‐nitrosylation of kainate‐type of ionotropic glutamate receptor 2 in epilepsy induced by kainic acid 下载免费PDF全文
Linxiao Wang Yanyan Liu Rulan Lu Guoying Dong Xia Chen Wenwei Yun Xianju Zhou 《Journal of neurochemistry》2018,144(3):255-270
6.
Adenosine A2A receptors are required for glutamate mGluR5‐ and dopamine D1 receptor‐evoked ERK1/2 phosphorylation in rat hippocampus: involvement of NMDA receptor 下载免费PDF全文
Paraskevi Krania Eleni Dimou Maria Bantouna Stylianos Kouvaros Eirini Tsiamaki Costas Papatheodoropoulos Konstantinos Sarantis Fevronia Angelatou 《Journal of neurochemistry》2018,145(3):217-231
7.
8.
A dual role for Integrin α6β4 in modulating hereditary neuropathy with liability to pressure palsies 下载免费PDF全文
Yannick Poitelon Vittoria Matafora Nicholas Silvestri Desirée Zambroni Claire McGarry Nora Serghany Thomas Rush Domenica Vizzuso Felipe A. Court Angela Bachi Lawrence Wrabetz Maria Laura Feltri 《Journal of neurochemistry》2018,145(3):245-257
9.
EphrinA/EphA‐dependent axon repulsion is crucial for synaptic targeting in developing neurons but downstream molecular mechanisms remain obscure. Here, it is shown that ephrinA5/EphA3 triggers proteolysis of the neural cell adhesion molecule (NCAM) by the metalloprotease a disintegrin and metalloprotease (ADAM)10 to promote growth cone collapse in neurons from mouse neocortex. EphrinA5 induced ADAM10 activity to promote ectodomain shedding of polysialic acid‐NCAM in cortical neuron cultures, releasing a ~ 250 kDa soluble fragment consisting of most of its extracellular region. NCAM shedding was dependent on ADAM10 and EphA3 kinase activity as shown in HEK293T cells transfected with dominant negative ADAM10 and kinase‐inactive EphA3 (K653R) mutants. Purified ADAM10 cleaved NCAM at a sequence within the E‐F loop of the second fibronectin type III domain (Leu671‐Lys672/Ser673‐Leu674) identified by mass spectrometry. Mutations of NCAM within the ADAM10 cleavage sequence prevented EphA3‐induced shedding of NCAM in HEK293T cells. EphrinA5‐induced growth cone collapse was dependent on ADAM10 activity, was inhibited in cortical cultures from NCAM null mice, and was rescued by WT but not ADAM10 cleavage site mutants of NCAM. Regulated proteolysis of NCAM through the ephrin5/EphA3/ADAM10 mechanism likely impacts synapse development, and may lead to excess NCAM shedding when disrupted, as implicated in neurodevelopmental disorders such as schizophrenia.
10.
Nicola J. Rutherford Brenda D. Moore Todd E. Golde Benoit I. Giasson 《Journal of neurochemistry》2014,131(6):859-867
The discoveries of mutations in SNCA were seminal findings that resulted in the knowledge that α‐synuclein (αS) is the major component of Parkinson's disease‐associated Lewy bodies. Since the pathologic roles of these protein inclusions and SNCA mutations are not completely established, we characterized the aggregation properties of the recently identified SNCA mutations, H50Q and G51D, to provide novel insights. The properties of recombinant H50Q, G51D, and wild‐type αS to polymerize and aggregate into amyloid were studied using (trans,trans)‐1‐bromo‐2,5‐bis‐(4‐hydroxy)styrylbenzene fluorometry, sedimentation analyses, electron microscopy, and atomic force microscopy. These studies showed that the H50Q mutation increases the rate of αS aggregation, whereas the G51D mutation has the opposite effect. However, H50Q and G51D αS could still be similarly induced to form intracellular aggregates from the exposure to exogenous amyloidogenic seeds under conditions that promote their cellular entry. Both mutant αS proteins, but especially G51D, promoted cellular toxicity under cellular stress conditions. These findings reveal that the novel pathogenic SNCA mutations, H50Q and G51D, have divergent effects on aggregation properties relative to the wild‐type protein, with G51D αS demonstrating reduced aggregation despite presenting with earlier disease onset, suggesting that these mutants promote different mechanisms of αS pathogenesis.
11.
Validated multi‐step approach for in vivo recording and analysis of optogenetically evoked glutamate in the mouse globus pallidus 下载免费PDF全文
Thomas Viereckel Åsa Konradsson‐Geuken Åsa Wallén‐Mackenzie 《Journal of neurochemistry》2018,145(2):125-138
12.
13.
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.
14.
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
15.
Lack of TNF‐alpha receptor type 2 protects motor neurons in a cellular model of amyotrophic lateral sclerosis and in mutant SOD1 mice but does not affect disease progression 下载免费PDF全文
Massimo Tortarolo Antonio Vallarola Dario Lidonnici Elisa Battaglia Gabriella Spaltro Fabio Fiordaliso Alessandro Corbelli Stefano Garetto Elisa Martini Laura Pasetto Marinos Kallikourdis Valentina Bonetto Caterina Bendotti 《Journal of neurochemistry》2015,135(1):109-124
Changes in the homeostasis of tumor necrosis factor α (TNFα) have been demonstrated in patients and experimental models of amyotrophic lateral sclerosis (ALS). However, the contribution of TNFα to the development of ALS is still debated. TNFα is expressed by glia and neurons and acts through the membrane receptors TNFR1 and TNFR2, which may have opposite effects in neurodegeneration. We investigated the role of TNFα and its receptors in the selective motor neuron death in ALS in vitro and in vivo. TNFR2 expressed by astrocytes and neurons, but not TNFR1, was implicated in motor neuron loss in primary SOD1‐G93A co‐cultures. Deleting TNFR2 from SOD1‐G93A mice, there was partial but significant protection of spinal motor neurons, sciatic nerves, and tibialis muscles. However, no improvement of motor impairment or survival was observed. Since the sciatic nerves of SOD1‐G93A/TNFR2?/? mice showed high phospho‐TAR DNA‐binding protein 43 (TDP‐43) accumulation and low levels of acetyl‐tubulin, two indices of axonal dysfunction, the lack of symptom improvement in these mice might be due to impaired function of rescued motor neurons. These results indicate the interaction between TNFR2 and membrane‐bound TNFα as an innovative pathway involved in motor neuron death. Nevertheless, its inhibition is not sufficient to stop disease progression in ALS mice, underlining the complexity of this pathology.
16.
David A. Davis Garnik Akopian John P. Walsh Constantinos Sioutas Todd E. Morgan Caleb E. Finch 《Journal of neurochemistry》2013,127(4):509-519
Airborne particulate matter (PM) from urban vehicular aerosols altered glutamate receptor functions and induced glial inflammatory responses in rodent models after chronic exposure. Potential neurotoxic mechanisms were analyzed in vitro. In hippocampal slices, 2 h exposure to aqueous nanosized PM (nPM) selectively altered post‐synaptic proteins in cornu ammonis area 1 (CA1) neurons: increased GluA1, GluN2A, and GluN2B, but not GluA2, GluN1, or mGlur5; increased post synaptic density 95 and spinophilin, but not synaptophysin, while dentate gyrus (DG) neurons were unresponsive. In hippocampal slices and neurons, MitoSOX red fluorescence was increased by nPM, implying free radical production. Specifically, N? production by slices was increased within 15 min of exposure to nPM with dose dependence, 1–10 μg/mL. Correspondingly, CA1 neurons exhibited increased nitrosylation of the GluN2A receptor and dephosphorylation of GluN2B (S1303) and of GluA1 (S831 & S845). Again, DG neurons were unresponsive to nPM. The induction of N? and nitrosylation were inhibited by AP5, an NMDA receptor antagonist, which also protects neurite outgrowth in vitro from inhibition by nPM. Membrane injury (EthidiumD‐1 uptake) showed parallel specificity. Finally, nPM decreased evoked excitatory post‐synaptic currents of CA1 neurons. These findings further document the selective impact of nPM on glutamatergic functions and identify novel responses of NMDA receptor‐stimulated N? production and nitrosylation reactions during nPM‐mediated neurotoxicity.
17.
Mature brain‐derived neurotrophic factor (mBDNF) plays a vital role in the nervous system, whereas proBDNF elicits neurodegeneration and neuronal apoptosis. Although current enzyme‐linked immunosorbent assay (ELISA) has been widely used to measure BDNF levels, it cannot differentiate mBDNF from proBDNF. As the function of proBDNF differs from mBDNF, it is necessary to establish an ELISA assay specific for the detection of mBDNF. Therefore, we aimed to establish a new mBDNF‐specific sandwich ELISA. In this study, we have screened and found a combination of antibodies for a sandwich ELISA. A monoclonal antibody and sheep anti‐BDNF were chosen as capture and detection antibody for sandwich ELISA respectively. The new ELISA showed no cross‐reactivity to human recombinant NT‐3, NT‐4, nerve growth factor and negligible cross‐reactivity (0.99–4.99%) for proBDNF compared to commercial ELISA kits (33.18–91.09%). The application of the new mBDNF ELISA was shown through the measurement of mBDNF levels in different brain regions of rats and in the brain of β‐site amyloid precursor protein cleaving enzyme 1 (BACE1)?/? and WT mice and compared to western blot. Overall, this new ELISA will be useful for the measurement of mBDNF levels with high specificity.
18.
Neuroprotective effects of Argon are mediated via an ERK‐1/2 dependent regulation of heme‐oxygenase‐1 in retinal ganglion cells 下载免费PDF全文
Felix Ulbrich Kai B. Kaufmann Mark Coburn Wolf Alexander Lagrèze Martin Roesslein Julia Biermann Hartmut Buerkle Torsten Loop Ulrich Goebel 《Journal of neurochemistry》2015,134(4):717-727
Retinal ischemia and reperfusion injuries (R‐IRI) damage neuronal tissue permanently. Recently, we demonstrated that Argon exerts anti‐apoptotic and protective properties. The molecular mechanism remains unclear. We hypothesized that Argon inhalation exert neuroprotective effects in rats retinal ganglion cells (RGC) via an ERK‐1/2 dependent regulation of heat‐shock proteins. Inhalation of Argon (75 Vol%) was performed after R‐IRI on the rats′ left eyes for 1 h immediately or with delay. Retinal tissue was harvested after 24 h to analyze mRNA and protein expression of heat‐shock proteins ?70, ?90 and heme‐oxygenase‐1, mitogen‐activated protein kinases (p38, JNK, ERK‐1/2) and histological changes. To analyze ERK dependent effects, the ERK inhibitor PD98059 was applicated prior to Argon inhalation. RGC count was analyzed 7 days after injury. Statistics were performed using anova . Argon significantly reduced the R‐IRI‐affected heat‐shock protein expression (p < 0.05). While Argon significantly induced ERK‐1/2 expression (p < 0.001), inhibition of ERK‐1/2 before Argon inhalation resulted in significantly lower vital RGCs (p < 0.01) and increase in heme‐oxygenase‐1 (p < 0.05). R‐IRI‐induced RGC loss was reduced by Argon inhalation (p < 0.001). Immunohistochemistry suggested ERK‐1/2 activation in Müller cells. We conclude, that Argon treatment protects R‐IRI‐induced apoptotic loss of RGC via an ERK‐1/2 dependent regulation of heme‐oxygenase‐1.
19.
Ethanol stimulates the in vivo axonal movement of neuropeptide dense‐core vesicles in Drosophila motor neurons 下载免费PDF全文