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Source: Journal of Molecular Neuroscience
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Total 63 results found since Jan 2013.
Mild Hypothermia Prevents NO-Induced Cytotoxicity in Human Neuroblastoma Cells Via Induction of COX-2
AbstractThe cold-inducible protein RBM3 mediates hypothermic neuroprotection against nitric oxide (NO)-induced cell death. Meanwhile, it is well-known that cyclooxygenase-2 (COX-2) is upregulated by RBM3 in several types of cells; however, it is still unclear whether COX-2 contributes to the neuroprotective effects of mild hypothermia/RBM3 against NO-induced cell death. Using human SH-SY5Y neuroblastoma cells, it was revealed that NO remarkably downregulates the expression of COX-2 at both mRNA and protein levels. When COX-2 was silenced using siRNA technique, cells became more sensitive to NO-induced cell death. Conversel...
Source: Journal of Molecular Neuroscience - November 23, 2018 Category: Neuroscience Source Type: research
Translocation Associated Membrane Protein 1 Contributes to Chronic Constriction Injury-Induced Neuropathic Pain in the Dorsal Root Ganglion and Spinal Cord in Rats
AbstractNeuropathic pain is a severe debilitating state caused by injury or dysfunction of somatosensory nervous system, and the clinical treatment is still challenging. Translocation associated membrane protein 1 (TRAM1), an adapter protein, participates in a variety of transduction pathways and mediates the biological functions such as cell proliferation, activation, and differentiation. However, whether TRAM1 is involved in the pathogenesis of neuropathic pain is still unclear. In our study, we reported the role of TRAM1 in the maintenance of neuropathic pain induced by chronic constriction injury (CCI) on rats. By west...
Source: Journal of Molecular Neuroscience - October 18, 2018 Category: Neuroscience Source Type: research
Biglycan, a Nitric Oxide-Downregulated Proteoglycan, Prevents Nitric Oxide-Induced Neuronal Cell Apoptosis via Targeting Erk1/2 and p38 Signaling Pathways
AbstractNitric oxide (NO), a gaseous signaling molecule, induces apoptosis and mediates neurodegenerative diseases and brain injury. Biglycan (BGN), a member of the small leucine-rich proteoglycan family, was demonstrated to exert anti-apoptosis function in various disease models. However, little is known about the effect of BGN on NO-induced neurotoxicity. Here, for the first time, we reported that BGN protects against NO-induced apoptosis in human neuroblastoma SH-EP1 cells. This is supported by the finding that sodium nitroprusside (SNP), a NO donor, triggered downregulation of BGN in SH-EP1 cells, and over-expression o...
Source: Journal of Molecular Neuroscience - August 7, 2018 Category: Neuroscience Source Type: research
ORL 1 Activation Mediates a Novel ORL 1 Receptor Agonist SCH221510 Analgesia in Neuropathic Pain in Rats
AbstractOpioid receptor like 1 (ORL1) receptor activation displayed an anti-nociceptive effect at spinal level for acute and neuropathic pain. SCH221510, an orally active non-peptide ORL1 agonist, was reported to be effective in treating neuropathic pain. The present study used ORL1 antagonist and siRNA to investigate that ORL1 activation mediates intrathecal SCH221510 analgesia in neuropathic pain induced by chronic constrictive injury (CCI) to rat sciatic nerve. Paw withdrawal latency and 50% mechanical threshold were measured for thermal and mechanical hypersensitivity in rats. CCI significantly decreased paw withdrawal...
Source: Journal of Molecular Neuroscience - August 3, 2018 Category: Neuroscience Source Type: research
Pre-Injection of Small Interfering RNA (siRNA) Promotes c-Jun Gene Silencing and Decreases the Survival Rate of Axotomy-Injured Spinal Motoneurons in Adult Mice
AbstractBrachial plexus injury is a common clinical peripheral nerve trauma. A series of genes in motoneurons were activated in the corresponding segments of the spinal cord after brachial plexus roots axotomy. The spatial and temporal expression of these genes directly affects the speed of motoneuron axon regeneration and precise target organ reinnervation. In a previous study, we observed the overexpression of c-Jun in motoneurons of the spinal cord ventral horn after brachial plexus injury in rats. However, the relevance of c-Jun expression with respect to the fate of axotomy-induced branchial plexus injury in adult mic...
Source: Journal of Molecular Neuroscience - July 10, 2018 Category: Neuroscience Source Type: research
Down-regulation of Long Noncoding RNA MALAT1 Protects Hippocampal Neurons Against Excessive Autophagy and Apoptosis via the PI3K/Akt Signaling Pathway in Rats with Epilepsy
In this study, we explore the ability of long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) to influence the autophagy and apoptosis of hippocampal neurons in epilepsy and the underlying mechanism involving the PI3K/Akt signaling pathway. Seventy-two Sprague-Dawley rats were assigned to normal, sham, Ep, Ep + si-NC, Ep + si-MALAT1, and Ep + si-MALAT1 + LY groups. Fluorescence in situ hybridization kit was employed to determine the MALAT1 in the brain tissues. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blotting were performed to determine the e...
Source: Journal of Molecular Neuroscience - June 1, 2018 Category: Neuroscience Source Type: research
Basic Fibroblast Growth Factor Protects Astrocytes Against Ischemia/Reperfusion Injury by Upregulating the Caveolin-1/VEGF Signaling Pathway
AbstractA previous in vivo study demonstrated that intracerebroventricular injection of basic fibroblast growth factor (bFGF) in middle cerebral artery occlusion rats increased the expression of caveolin-1 (cav-1) and vascular endothelial growth factor (VEGF) in cerebral ischemia penumbra. Because astrocytes are the largest population in the brain, the aim of this in vitro study was to investigate the influence of bFGF on cav-1 and VEGF expression in rat astrocytes following oxygen glucose deprivation/reoxygenation (OGD/R). For this, an ischemic model in vitro of oxygen glucose deprivation lasting for 6 h, followed by 24...
Source: Journal of Molecular Neuroscience - January 3, 2018 Category: Neuroscience Source Type: research
Suppression of Disheveled –Axin Domain Containing 1 (DIXDC1) by MicroRNA-186 Inhibits the Proliferation and Invasion of Retinoblastoma Cells
In this study, we aimed to investigate the biological function of DIDXDC1 in RB and the way in which its expression is regulated by microRNAs (miRNAs). We foun d that DIXDC1 expression was significantly upregulated in RB cell lines. The silencing of DIXDC1 by small interfering RNA (siRNA) significantly inhibited the proliferation, invasion, and Wnt signaling in RB cell lines. Interestingly, DIXDC1 was identified as a target gene of miR-186. The expression of DIXDC1 was negatively regulated by miR-186, and DIXDC1 expression was inversely correlated with miR-186 expression in RB clinical specimens. Overexpression of miR-186 ...
Source: Journal of Molecular Neuroscience - December 20, 2017 Category: Neuroscience Source Type: research
Let-7d microRNA Attenuates 6-OHDA-Induced Injury by Targeting Caspase-3 in MN9D Cells
AbstractParkinson ’s disease (PD) mainly results from the progressive loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc), and the exact underlying mechanisms of the loss of DA neurons in PD remains largely unclear. The results of our previous work showed that let-7d was significantly dow nregulated in a 6-OHDA-induced cellular model of PD. However, the exact effect of let-7d on DA neural cells was unclear. In MN9D dopaminergic neuronal cells, we used a let-7d mimic and inhibitor to upregulate and downregulate the expression of let-7d, respectively, a cell counting kit to assess cell viability,...
Source: Journal of Molecular Neuroscience - October 29, 2017 Category: Neuroscience Source Type: research
Mfn2-Mediated Preservation of Mitochondrial Function Contributes to the Protective Effects of BHAPI in Response to Ischemia
This study investigated the protective effects of N ′-(1-(2-((4-(4,4,5,5-tetramethyl-1,2,3-dioxoborolan-2-yl)benzyl)oxy)phenyl)ethylidene (BHAPI) on an in vitro ischemia model mimicked by oxygen and glucose deprivation (OGD) in neuronal HT22 cells. The results showed that BHAPI significantly increased cell viability and decreased lactate dehydrogen ase (LDH) release after OGD. BHAPI treatment also reduced apoptosis, as measured by flow cytometry, and suppressed caspase-3 activation. These protective effects were accompanied by preserved mitochondrial membrane potential (MMP), reduced mitochondrial swelling, promoted mito...
Source: Journal of Molecular Neuroscience - September 26, 2017 Category: Neuroscience Source Type: research
Vimentin Promotes Astrocyte Activation After Chronic Constriction Injury
In this study, the role of vimentin in chronic constriction injury (CCI) was investigated. Western blot revealed increased protein level of vimentin following CCI, peaking at 7 days. Double immunofluorescent staining showed that vimentin was mostly co-localized with astrocytes, not with neurons or microglia. In vitro, sensory neuronal injury stimulated astrocytes to produce more pro-inflammation cytokines, p-ERK (phosphorylated extracellular signal-regulated protein kina se), and vimentin. However, vimentin knockdown by siRNA (small interfering RNA) reversed the upregulation of p-ERK and vimentin expression and reduced t...
Source: Journal of Molecular Neuroscience - August 8, 2017 Category: Neuroscience Source Type: research
The Involvement of NR2B and tau Protein in MG132-Induced CREB Dephosphorylation
AbstractTranscription factor cAMP response element-binding protein (CREB) plays a critical role in memory formation. Ubiquitin-proteasome system-dependent protein degradation affects the upstream signaling pathways which regulate CREB activity. However, the molecular mechanisms of proteasome inhibition on reductive CREB activity are still unclear. The current study demonstrated that MG132-inhibited proteasome activity resulted in a dose dependence of CREB dephosphorylation at Ser133 as well as decreased phosphorylation ofN-methyl-d-aspartate (NMDA) receptor subunit NR2B (Tyr1472) and its tyrosine protein kinase Fyn (Tyr416...
Source: Journal of Molecular Neuroscience - April 19, 2017 Category: Neuroscience Source Type: research
Neuroprotective Role of Exogenous Brain-Derived Neurotrophic Factor in Hypoxia –Hypoglycemia-Induced Hippocampal Neuron Injury via Regulating Trkb/MiR134 Signaling
AbstractHypoxic –ischemic brain injury is an important cause of neonatal mortality and morbidity. Brain-derived neurotrophic factor (BDNF) has been reported to play a neuroprotective role in hypoxic–ischemic brain injury; however, the specific effects and mechanism of BDNF on hypoxic–hypoglycemic hippocampal neuron injury remains unknown. The current study investigated the action of BDNF in regulating cerebral hypoxic-ischemic injury by simulating hippocampal neuron ischemia and hypoxia. We found that BDNF, p-Trkb, and miR-134 expression levels decreased, and that exogenous BDNF increased survival and r educed apopto...
Source: Journal of Molecular Neuroscience - March 26, 2017 Category: Neuroscience Source Type: research
NFAT5 protects astrocytes against oxygen –glucose–serum deprivation/restoration damage via the SIRT1/Nrf2 pathway
In this study, our aim is to investigate whether NFAT5 overexpression can protect astrocytes against oxygen –glucose–serum deprivation/restoration (OGSD/R) damage. In vivo, rats were subjected to ischemia–reperfusion injury, resulting in increased water content, infarct volume, and expression of NFAT5 protein in rat spinal cord. After primary culture for spinal cord astrocytes, the in vitro OGSD/R m odel was established. The results of the CCK8 assay and flow cytometry showed that, in the OGSD/R group, astrocyte cell viability was downregulated, but astrocyte apoptosis increased. Caspase 3 activity increased as well....
Source: Journal of Molecular Neuroscience - November 11, 2016 Category: Neuroscience Source Type: research
Role of Nectin-1/c-Src Signaling in the Analgesic Effect of GDNF on a Rat Model of Chronic Constrictive Injury
In this study, we aimed to examine whether the adhesion protein nectin-1 and its downstream protein c-Src are involved in neuropathic pain. We found that nectin-1 was expressed in the superficial dorsal horn of the spinal cord and that it was increased after chronic constrictive injury (CCI). Intrathecal administration of nectin-1 siRNA attenuated neuropathic pain induced by CCI via interference of the expression of nectin-1. Furthermore, we found that GDNF can downregulate the phosphorylation level of nectin-1-associated c-Src without changing the expression level of nectin-1. In summary, these data suggest that nectin-1 ...
Source: Journal of Molecular Neuroscience - July 8, 2016 Category: Neuroscience Source Type: research
