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Source: Molecular Neurobiology
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Total 171 results found since Jan 2013.

Knockdown of Astrocytic Monocarboxylate Transporter 4 in the Motor Cortex Leads to Loss of Dendritic Spines and a Deficit in Motor Learning
In this study, we investigated astrocyte-specific MCT4 in motor learning and neuroplasticity of the M1 primary motor cortex using a cell-type specific shRNA knockdown of MCT4. Knockdown of astrocyte-specific MCT4 resulted in impaired motor performance and learning on the accelerating rotarod. In addition, MCT4 knockdown was associated with a reduction of neuronal dendritic spine density and spine width and decreased protein expression of PSD95, Arc, and cFos. Using near-infrared –conjugated 2-deoxyglucose uptake as a surrogate marker for neuronal activity, MCT4 knockdown was also associated with decreased neuronal activi...
Source: Molecular Neurobiology - November 25, 2021 Category: Neurology Source Type: research

COX-2/PGE2 Pathway Inhibits the Ferroptosis Induced by Cerebral Ischemia Reperfusion
In conclusion, PGE2 was positively correlated with ferroptosis, inhibition of ferroptosis induced by cerebral I/R can inactivate COX-2/PGE2 pathway, and PGE2 inhibited ferroptosis induced by cerebral I/R, possibly via PGE2 receptor 3 and PGE2 receptor 4.Graphical abstractInhibition of ferroptosis inactivates the COX-2/PGE2 pathway. Cerebral ischemia reperfusion injury induces the secretion of PGE2. After the inhibition of ferroptosis by Fer-1, the expression of cyclooxygenases (COX-1 and COX-2) decreased, and PGE2 synthases cPGES, mPGES-1, and mPGES-2 were also reduced. At the same time, the PGE2 degradation enzyme 15-PGDH...
Source: Molecular Neurobiology - January 10, 2022 Category: Neurology Source Type: research

Sevoflurane Offers Neuroprotection in a Cerebral Ischemia/Reperfusion Injury Rat Model Through the E2F1/EZH2/TIMP2 Regulatory Axis
This study is aimed to delineate the molecular mechanistic actions by which sevoflurane protects against cerebral I/R injury. A rat model of cerebral I/R injury was established and pre-treated with sevoflurane, in which hippocampal neuron apoptosis was found to be repressed and the level of E2F transcription factor 1 (E2F1) was observed to be down-regulated. Then, the up-regulated expression of E2F1 was validated in rats with cerebral I/R injury, responsible for stimulated neuron apoptosis. Further, the binding of E2F1 to enhancer of zeste homolog 2 (EZH2) and EZH2 to tissue inhibitor of metalloproteinases-2 (TIMP2) was id...
Source: Molecular Neurobiology - January 22, 2022 Category: Neurology Source Type: research

The Two-Pore Domain Potassium Channel TREK-1 Promotes Blood –Brain Barrier Breakdown and Exacerbates Neuronal Death After Focal Cerebral Ischemia in Mice
This study used TREK-1-deficient mice to directly investigate the role of TREK-1 after focal cerebral ischemia. First, immunofluorescence assays in the mouse cerebral cortex indicated that TREK-1 expression was mostly abundant in astrocytes, neurons, and oligodendrocyte precursor cells but was low in myelinating oligodendrocytes, microglia, or endothelial cells. TREK-1 deficiency did not affect brain weight and morphology or the number of neurons, astrocytes, or microglia but did increase glial fibrillary acidic protein (GFAP) expression in astrocytes of the cerebral cortex. The anatomy of the major cerebral vasculature, n...
Source: Molecular Neurobiology - January 24, 2022 Category: Neurology Source Type: research

Imeglimin Is Neuroprotective Against Ischemic Brain Injury in Rats —a Study Evaluating Neuroinflammation and Mitochondrial Functions
This study demonstrates that post-stroke treatment with imeglimin exerts neuroprotec tive effects by reducing infarct size and neuronal loss possibly via the resolution of neuroinflammation and partly via inhibition of mPTP opening in neurons and astrocytes.Graphical abstract
Source: Molecular Neurobiology - March 7, 2022 Category: Neurology Source Type: research

Astrocyte-Derived TNF- α-Activated Platelets Promote Cerebral Ischemia/Reperfusion Injury by Regulating the RIP1/RIP3/AKT Signaling Pathway
In this study, we created an I/R mouse model via middle cerebral artery occlusion and reperfusion (MCAO/R) and analyzed the transcriptomic profiles of the ipsilateral and contralateral cortices using RNA-seq. We found that cerebral I/R injury induced platelet invasion and accumulation in the cerebral cortex by stimulating TNF- α secretion from activated astrocytes in the ischemic region, while TNF-α expression enhanced platelet reactivity through the RIP1/RIP3/AKT pathway. Furthermore, the inoculation of TNF-α-stimulated platelets aggravated I/R injury in mice, whereas the administration of anti-TNF-α antibodies at th ...
Source: Molecular Neurobiology - July 4, 2022 Category: Neurology Source Type: research

miR-383-5p Regulated by the Transcription Factor CTCF Affects Neuronal Impairment in Cerebral Ischemia by Mediating Deacetylase HDAC9 Activity
AbstractStroke, the leading cause of long-term disability worldwide, is caused by the blockage or hemorage of cerebral arteries. The resultant cerebral ischemia causes local neuronal death and brain injury. Histone deacetylase 9 (HDAC9) has been reported to be elevated in ischemic brain injury, but its mechanism in stroke is still enigmatic. The present study aimed to unveil the manner of regulation of HDAC9 expression and the effect of HDAC9 activation on neuronal function in cerebral ischemia. MicroRNAs (miRNAs) targeting HDAC9 were predicted utilizing bioinformatics analysis. We then constructed the oxygen glucose depri...
Source: Molecular Neurobiology - August 4, 2022 Category: Neurology Source Type: research

Investigation of Mitochondrial Related Variants in a Cerebral Small Vessel Disease Cohort
AbstractMonogenic forms of cerebral small vessel disease (CSVD) can be caused by both variants in nuclear DNA and mitochondrial DNA (mtDNA). Mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) is known to have a phenotype similar to Cerebral Autosomal Dominant Arteriopathy with Sub-cortical Infarcts and Leukoencephalopathy (CADASIL), and can be caused by variants in the mitochondrial genome and in several nuclear-encoded mitochondrial protein (NEMP) genes. The aim of this study was to screen for variants in the mitochondrial genome and NEMP genes in aNOTCH3-negative CADASIL cohort, to identify a...
Source: Molecular Neurobiology - August 23, 2022 Category: Neurology Source Type: research

Astrocyte-Derived TNF- α-Activated Platelets Promote Cerebral Ischemia/Reperfusion Injury by Regulating the RIP1/RIP3/AKT Signaling Pathway
In this study, we created an I/R mouse model via middle cerebral artery occlusion and reperfusion (MCAO/R) and analyzed the transcriptomic profiles of the ipsilateral and contralateral cortices using RNA-seq. We found that cerebral I/R injury induced platelet invasion and accumulation in the cerebral cortex by stimulating TNF- α secretion from activated astrocytes in the ischemic region, while TNF-α expression enhanced platelet reactivity through the RIP1/RIP3/AKT pathway. Furthermore, the inoculation of TNF-α-stimulated platelets aggravated I/R injury in mice, whereas the administration of anti-TNF-α antibodies at th ...
Source: Molecular Neurobiology - August 25, 2022 Category: Neurology Source Type: research

Transcranial Direct-Current Stimulation Regulates MCT1-PPA-PTEN-LONP1 Signaling to Confer Neuroprotection After Rat Cerebral Ischemia –Reperfusion Injury
This study supports a potential application of tDCS in ischemic stroke.
Source: Molecular Neurobiology - October 29, 2022 Category: Neurology Source Type: research

Amorfrutin B Protects Mouse Brain Neurons from Hypoxia/Ischemia by Inhibiting Apoptosis and Autophagy Processes Through Gene Methylation- and miRNA-Dependent Regulation
Abstract Amorfrutin B is a selective modulator of the PPAR γ receptor, which has recently been identified as an effective neuroprotective compound that protects brain neurons from hypoxic and ischemic damage. Our study demonstrated for the first time that a 6-h delayed post-treatment with amorfrutin B prevented hypoxia/ischemia-induced neuronal apoptosis i n terms of the loss of mitochondrial membrane potential, heterochromatin foci formation, and expression of specific genes and proteins. The expression of all studied apoptosis-related factors was decreased in response to amorfrutin B, both during hypoxia and ischemia,...
Source: Molecular Neurobiology - January 19, 2023 Category: Neurology Source Type: research