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The Weakened Interaction Between HECTD4 and GluN2B in Ischemic Stroke Promotes Calcium Overload and Brain Injury Through a Mechanism Involving the Decrease of GluN2B and MALT1 Ubiquitination
This study explores the relationship between HECTD4, GluN2B, and MALT1, focusing on their role in brain injury in ischemic stroke. Rats were subjected to 2  h-ischemia followed by 24-h reperfusion to establish an ischemic stroke model. We observed the downregulation of HECTD4 and the upregulation of MALT1. Additionally, an increased GluN2B phosphorylation was concomitant with weakened interactions between HECTD4 and GluN2B, followed by decreased stria tal-enriched protein phosphatase (STEP61). Knockdown of HECTD4 exacerbated hypoxia- or NMDA-induced injury in nerve cells coincident with a decrease in GluN2B and MALT1 ubiq...
Source: Molecular Neurobiology - February 4, 2023 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

Role of tRNA-Derived Fragments in Neurological Disorders: a Review
AbstracttRFs are small tRNA derived fragments that are emerging as novel therapeutic targets and regulatory molecules in the pathophysiology of various neurological disorders. These are derived from precursor or mature tRNA, forming different subtypes that have been reported to be involved in neurological disorders like stroke, Alzheimer ’s, epilepsy, Parkinson’s, MELAS, autism, and Huntington’s disorder. tRFs were earlier believed to be random degradation debris of tRNAs. The significant variation in the expression level of tRFs in disease conditions indicates their salient role as key players in regulation of these...
Source: Molecular Neurobiology - January 19, 2023 Category: Neurology Source Type: research

Spinal MCP-1 Contributes to Central Post-stroke Pain by Inducing Central Sensitization in Rats
In this study, rats were subjected to thalamic hemorrhage to investigate the role of spinal monocyte chemoattractant protein-1 (MCP-1) and C-C motif chemokine receptor 2 (CCR2) in the development of CPSP. Immunohistochemical staining and ELISA were used to assess the expression changes of c-Fos, Iba-1, GFAP, MCP-1, and CCR2 in the dorsal horn of the lumbar spinal cord following thalamic hemorrhage, and the involvement of spinal MCP-1 in CPSP was examined by performing intrathecal anti-MCP-1 mAb injection to neutralize the spinal extracellular MCP-1. We demonstrated that intra-thalamic collagenase microinjection induced per...
Source: Molecular Neurobiology - January 5, 2023 Category: Neurology Source Type: research

BMSC-Derived Exosomal Egr2 Ameliorates Ischemic Stroke by Directly Upregulating SIRT6 to Suppress Notch Signaling
AbstractExosomes generated by BMSCs contribute to functional recovery in ischemic stroke. However, the regulatory mechanism is largely unknown. Exosomes were isolated from BMSCs. Tube formation, MTT, TUNEL, and flow cytometry assays were applied to examine cell angiogenesis, viability, and apoptosis. Protein and DNA interaction was evaluated by ChIP and luciferase assays. LDH release into the culture medium was examined. Infarction area was evaluated by TTC staining. Immunofluorescence staining was applied to examine CD31 expression. A mouse model of MCAO/R was established. BMSC-derived exosomes attenuated neuronal cell da...
Source: Molecular Neurobiology - December 17, 2022 Category: Neurology Source Type: research

SATB1/SLC7A11/HO-1 Axis Ameliorates Ferroptosis in Neuron Cells After Ischemic Stroke by Danhong Injection
AbstractNeuronal damage after ischemic stroke (IS) is frequently due to ferroptosis, contributing significantly to ischemic injury. However, the mechanism against ferroptosis in IS remained unclear. The aim of this study was to investigate the potential mechanism of Danhong injection (DHI) and the critical transcription factor SATB1 in preventing neuronal ferroptosis after ischemic stroke in vivo and in vitro. The results showed that DHI treatment significantly reduced the infarct area and associated damage in the brains of the pMCAO mice, and enhanced the viability of OGD-injured neurons. And several characteristic indica...
Source: Molecular Neurobiology - December 17, 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 - December 1, 2022 Category: Neurology Source Type: research

Silencing of Long Noncoding RNA GAS5 Blocks Experimental Cerebral Ischemia –Reperfusion Injury by Restraining AQP4 Expression via the miR-1192/STAT5A Axis
This study aimed to elucidate the regulatory mechanism of the lncRNA GAS5 on STAT5A in cerebral ischemia/reperfusion (I/R) injury. First, GAS5 and STAT5A levels in the blood of patients with stroke were determined. Then, a middle cerebral artery occlusion and reperfusion rat model was established in which short hairpin RNAs targeting GAS5 or STAT5A were intracranially injected, followed by the assessment of neurological function, cerebral injury and water content, and inflammation. Primary rat astrocytes were induced with oxygen –glucose deprivation/reoxygenation (OGD/R), and cell proliferation, apoptosis, and inflammati...
Source: Molecular Neurobiology - October 29, 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 25, 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

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

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

Paracrine Effects of Mesenchymal Stem Cells in Ischemic Stroke: Opportunities and Challenges
AbstractIt is well acknowledged that neuroprotective effects of transplanted mesenchymal stem cells (MSCs) in ischemic stroke are attributed to their paracrine-mediated actions or bystander effects rather than to cell replacement in infarcted areas. This therapeutic plasticity is due to MSCs ’ ability to secrete a broad range of bioactive molecules including growth factors, trophic factors, cytokines, chemokines, and extracellular vesicles, overall known as the secretome. The secretome derivatives, such as conditioned medium (CM) or purified extracellular vesicles (EVs), exert remarka ble advantages over MSC transplantat...
Source: Molecular Neurobiology - August 3, 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

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