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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

Role of PDGF-A-Activated ERK Signaling Mediated FAK-Paxillin Interaction in Oligodendrocyte Progenitor Cell Migration
AbstractOligodendrocyte progenitor cells (OPCs) originate from the sub-ventricular zone of the developing brain. They migrate and proliferate to occupy the white matter tracts of the central nervous system and transform into myelinating oligodendrocytes. Along their route of migration, OPCs are guided and controlled by several growth factors and chemokines. PDGF-A (platelet-derived growth factor), a growth factor, serves as a monogenic and mitogenic cue during the process and activates intracellular signaling pathways inside the cell. Activation of extracellular signal regulated kinase (ERK) signaling is one of the mechani...
Source: Journal of Molecular Neuroscience - January 16, 2019 Category: Neuroscience Source Type: research

Inhibition of MSK1 Promotes Inflammation and Apoptosis and Inhibits Functional Recovery After Spinal Cord Injury
In this study, we found that MSK1 is gradually decreased, starting 1  day after spinal cord injury and to its lowest level 3 days post-injury, after which it gradually increased. To further investigate the possible function of MSK1 in spinal cord injury, we interfered with its expression by utilizing a small interfering RNA (siRNA)-encoding lentivirus, which was in jected into the injured spinal cord to inhibit local expression. After MSK1 inhibition, we found that the expression of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β were increased. Moreover, the expression of IL-10 was decreased. In addition,...
Source: Journal of Molecular Neuroscience - March 26, 2019 Category: Neuroscience Source Type: research

Euxanthone Ameliorates Sevoflurane-Induced Neurotoxicity in Neonatal Mice
This study was designed to investigate whether euxanthone can confer neuroprotective activities against sevoflurane-induced neurotoxicity and to determine the associated molecular mechanisms. Neonatal Sprague-Dawley (male) rats were exposed to sevoflurane with or without euxanthone treatment. The behavioral data of rats were collected at P41 (the beginning of the adult stage). The hippocampal tissue was obtained following exposure to sevoflurane. The reactive oxygen species (ROS) level in the hippocampal tissue was determined by a commercial kit. The expression of apoptotic markers and inflammatory cytokines was determined...
Source: Journal of Molecular Neuroscience - March 29, 2019 Category: Neuroscience Source Type: research

Downregulation of AIF-2 Inhibits Proliferation, Migration, and Invasion of Human Glioma Cells via Mitochondrial Dysfunction
In conclusion, we found that AIF-2 plays a key role in promoting cell proliferation, invasion, and migration via regulating AIF-1-related mitochondrial cascades. Downregulation of the candidate oncogene AIF-2 might constitute a strategy to kill human glioma cells.
Source: Journal of Molecular Neuroscience - April 12, 2019 Category: Neuroscience Source Type: research

Nrf2 Mediates the Anti-apoptotic and Anti-inflammatory Effects Induced by Gastrodin in Hydrogen Peroxide –Treated SH-SY5Y Cells
AbstractRedox impairment, inflammation, and increased rates of cell death are central players during neurodegeneration. In that context, activation of the transcription factor nuclear factor erythroid 2 –related factor 2 (Nrf2) has been viewed as an interesting strategy in order to reduce the impact of redox dysfunction and neuroinflammation on cell fate. There is evidence indicating that the benefits caused by natural products in the brain may be due to the ability of these agents in upregulatin g Nrf2. Gastrodin (GAS) induces anti-oxidant, anti-inflammatory, and anti-apoptotic actions in brain cells. Nonetheless, the m...
Source: Journal of Molecular Neuroscience - May 26, 2019 Category: Neuroscience Source Type: research

Oxygen-Glucose Deprivation/Reoxygenation Induces Human Brain Microvascular Endothelial Cell Hyperpermeability Via VE-Cadherin Internalization: Roles of RhoA/ROCK2
In conclusion, the present study provides evidence that OGD/R may induce HBMEC monolayer hyperpermeability via RhoA/ROCK2-mediated VE-cadherin internalization, which may provide an impetus for the development of therapeutics targeting BBB damage in ischemic stroke.
Source: Journal of Molecular Neuroscience - June 10, 2019 Category: Neuroscience Source Type: research

MicroRNA-326 Inhibits Apoptosis and Promotes Proliferation of Dopaminergic Neurons in Parkinson ’s Disease Through Suppression of KLK7-Mediated MAPK Signaling Pathway
AbstractParkinson ’s disease (PD), one of the motor system disorders, is characterized by the loss of dopamine-producing brain cells. Accumulating evidence has highlighted the involvement of microRNAs (miRs) in the development and progression of PD. Hence, we aimed at exploring possible effects of miR-326 on the pr ogression of PD in mice in an attempt to elucidate the underlying mechanism associated with the kallikrein-related peptidase 7 (KLK7)–mediated mitogen-activated protein kinase (MAPK) signaling pathway. In order to identify the regulatory relationship between miR-326 and KLK7 and its biological sig nificance ...
Source: Journal of Molecular Neuroscience - July 2, 2019 Category: Neuroscience Source Type: research

Knockdown of MCM10 Gene Impairs Glioblastoma Cell Proliferation, Migration and Invasion and the Implications for the Regulation of Tumorigenesis
AbstractMinichromosome maintenance 10 (MCM10) plays an important role in DNA replication and is expressed in a variety of tumors, including glioma. However, its role and mechanism in glioma remain elusive. The purpose of this study was to examine the molecular function of MCM10 in glioblastoma cell lines in vitro and to further investigate the molecular mechanisms in the network mediated by MCM10. Cell proliferation, invasion, and migration were investigated in the absence of MCM10 mediated by RNA interference (RNAi) in U87 and U251 cell lines. Microarray data were obtained from U87 cells infected with a lentivirus express...
Source: Journal of Molecular Neuroscience - February 5, 2020 Category: Neuroscience Source Type: research

Induction of SPARC on Oxidative Stress, Inflammatory Phenotype Transformation, and Apoptosis of Human Brain Smooth Muscle Cells Via TGF- β1-NOX4 Pathway
AbstractSecreted protein acidic and rich in cysteine (SPARC) has a close association with inflammatory response and oxidative stress in tissues and is widely expressed in intracranial aneurysms (IAs), especially in smooth muscle cells. Therefore, it is inferred that SPARC might be involved in the formation and development of IAs through the inflammatory response pathway or oxidative stress pathway. The aim of this study is to investigate the pathological mechanism of SPARC in oxidative stress, inflammation, and apoptosis during the formation of IAs, as well as the involvement of TGF- β1 and NOX4 molecules. Human brain vas...
Source: Journal of Molecular Neuroscience - June 2, 2020 Category: Neuroscience Source Type: research

Cadaverine and Spermine Elicit Ca 2+ Uptake in Human CP Cells via a Trace Amine-Associated Receptor 1 Dependent Pathway
AbstractThe choroid plexus (CP) constitutes a barrier between the blood and the cerebrospinal fluid (CSF) which regulates the exchange of substances between these two fluids through mechanisms that are not completely understood. Polyamines as spermine, spermidine and putrescine are produced by all cells and are present in the CSF. Interestingly, their levels are altered in some neuronal disorders as Alzheimer ’s and Parkinson’s diseases, thus increasing the interest in their signalling in the central nervous system (CNS). Cadaverine, on the other hand, is synthetized by the intestinal microbiome, suggesting that the pr...
Source: Journal of Molecular Neuroscience - August 19, 2020 Category: Neuroscience Source Type: research

Caffeine Inhibits Activation of the NLRP3 Inflammasome via Autophagy to Attenuate Microglia-Mediated Neuroinflammation in Experimental Autoimmune Encephalomyelitis
This study examined the mechanism underlying the anti-inflammatory effect of caffeine on EAE. In this study, C57BL/6 mice were immunized  to induce EAE and treated with caffeine to observe its effect on prognosis. The effects of caffeine on autophagy and inflammation were also analysed in mouse primary microglia (PM) and the BV2 cell line. The data demonstrated that caffeine reduced the clinical score, the infiltration of inflammat ory cells, the demyelination level, and the activation of microglia in EAE mice. Furthermore, caffeine increased the LC3-II/LC3-I levels and decreased the NLRP3 and P62 levels in EAE mice, whe...
Source: Journal of Molecular Neuroscience - September 3, 2021 Category: Neuroscience Source Type: research

MiR-124 Prevents the Microglial Proinflammatory Response by Inhibiting the Activities of TLR4 and Downstream NLRP3 in Palmitic Acid-Treated BV2 Cells
AbstractNeuroinflammation is a mechanism by which obesity or a high-fat diet leads to cognitive impairment. MiR-124, a highly expressed microRNA in the brain, can alleviate neuroinflammation by regulating microglial activation, but its mechanism is unclear. The aim of the study was to explore whether miR-124 exerted this effect through TLR4/MyD88/NF- κB p65/NLRP3 signaling in palmitic acid-treated BV2 cells. Prepared BV2 cells were treated with palmitic acid to establish an in vitro model of a high-fat diet. An miR-124 mimic and inhibitor were adopted to upregulate and downregulate the expression of miR-124, respectively....
Source: Journal of Molecular Neuroscience - October 15, 2021 Category: Neuroscience Source Type: research

TRPV1 Suppressed NLRP3 Through Regulating Autophagy in Microglia After Ischemia-Reperfusion Injury
This study aimed to investigate whether autophagy regulates inflammatory is associated with TRPV1. Model of oxygen and glucose deprivation/reoxygenation (OGD/R) was established in vitro to induce cerebral ischemia-reperfusion injury (I/R). siRNA of Atg5, inhibitors, and agonists of both autophagy and TRPV1 were involved in our study. Autophagy was assayed by immunofluorescence staining LC-3 and autophagosome was observed using transmission electron microscopy (TEM). Autophagy/inflammation-related markers as Atg5, LC-3II/LC-3I, Beclin-1, NLRP3, IL-1 β, and Caspase-1 were also measured in the present study. Results indicate...
Source: Journal of Molecular Neuroscience - January 18, 2022 Category: Neuroscience Source Type: research