0000000000225833

AUTHOR

Changsheng Huang

0000-0003-0535-1865

showing 5 related works from this author

SETD7 mediates spinal microgliosis and neuropathic pain in a rat model of peripheral nerve injury

2019

Abstract Gene transcription regulation is critical for the development of spinal microgliosis and neuropathic pain after peripheral nerve injury. Using a model of chronic constriction injury (CCI) of the sciatic nerve, this study characterized the role of SET domain containing lysine methyltransferase 7 (SETD7) which monomethylates histone H3 lysine 4 (H3K4me1), a marker for active gene transcription. SETD7 protein expression in the spinal dorsal horn ipsilateral to nerve lesion was increased from one day to 14 days after CCI, concomitantly with the expression of inflammatory genes, Ccl2, Il-6 and Il-1β. The CCI-induced SETD7 expression was predominantly localized to microglia, as demonstra…

Male0301 basic medicineSpinal Cord Dorsal HornPathologymedicine.medical_specialtyImmunologyCCL2MicrogliosisRats Sprague-Dawley03 medical and health sciencesBehavioral Neuroscience0302 clinical medicinePeripheral Nerve InjuriesGanglia SpinalmedicineAnimalsGene knockdownMicrogliaEndocrine and Autonomic Systemsbusiness.industryHistone-Lysine N-MethyltransferaseNerve injurySciatic NerveSpineRats030104 developmental biologymedicine.anatomical_structureSpinal CordHyperalgesiaNeuropathic painPeripheral nerve injuryNeuralgiaFemaleMicrogliaSciatic nervemedicine.symptombusiness030217 neurology & neurosurgeryBrain, Behavior, and Immunity
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Lack of NG2 exacerbates neurological outcome and modulates glial responses after traumatic brain injury

2015

Traumatic brain injury (TBI) is a major cause of death and disability. The underlying pathophysiology is characterized by secondary processes including neuronal death and gliosis. To elucidate the role of the NG2 proteoglycan we investigated the response of NG2-knockout mice (NG2-KO) to TBI. Seven days after TBI behavioral analysis, brain damage volumetry and assessment of blood brain barrier integrity demonstrated an exacerbated response of NG2-KO compared to wild-type (WT) mice. Reactive astrocytes and expression of the reactive astrocyte and neurotoxicity marker Lcn2 (Lipocalin-2) were increased in the perilesional brain tissue of NG2-KO mice. In addition, microglia/macrophages with acti…

0301 basic medicinePathologymedicine.medical_specialtyMicrogliaTraumatic brain injurybusiness.industryNeurotoxicityPoison controlBrain damagemedicine.diseaseBlood–brain barrier03 medical and health sciencesCellular and Molecular Neuroscience030104 developmental biologymedicine.anatomical_structurenervous systemNeurologyGliosisImmunologymedicineNeurogliamedicine.symptombusinessGlia
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Influence of Age on Brain Edema Formation, Secondary Brain Damage and Inflammatory Response after Brain Trauma in Mice

2012

After traumatic brain injury (TBI) elderly patients suffer from higher mortality rate and worse functional outcome compared to young patients. However, experimental TBI research is primarily performed in young animals. Aim of the present study was to clarify whether age affects functional outcome, neuroinflammation and secondary brain damage after brain trauma in mice. Young (2 months) and old (21 months) male C57Bl6N mice were anesthetized and subjected to a controlled cortical impact injury (CCI) on the right parietal cortex. Animals of both ages were randomly assigned to 15 min, 24 h, and 72 h survival. At the end of the observation periods, contusion volume, brain water content, neurolo…

MalePathologyAgingAnatomy and PhysiologyCritical Care and Emergency MedicineMouseT-LymphocytesInterleukin-1beta610 MedizinNitric Oxide Synthase Type IISystemic inflammationMiceAnesthesiologyCell Movement610 Medical sciencesEdemaImmune PhysiologyEdemaLungNeurosurgical CareMultidisciplinaryHematologic TestsQRAging and ImmunityAnimal ModelsOrgan SizeHead Injurymedicine.anatomical_structureNeurologyNeurointensive CareCytokinesMedicinemedicine.symptomResearch Articlemedicine.medical_specialtyTraumatic brain injuryScienceImmunologyInflammationBrain damageAtrophyModel OrganismsNeurorehabilitation and TraumamedicineAnimalsRNA MessengerBiologyCerebrumNeuroinflammationInflammationLungbusiness.industryInterleukin-6Tumor Necrosis Factor-alphaImmunityWatermedicine.diseaseMice Inbred C57BLGene Expression RegulationCyclooxygenase 2Immune SystemBrain InjuriesClinical ImmunologybusinessPhysiological ProcessesPLoS ONE
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Targeting aurora kinase B alleviates spinal microgliosis and neuropathic pain in a rat model of peripheral nerve injury.

2019

Peripheral nerve injury elicits spinal microgliosis, contributing to neuropathic pain. The aurora kinases A (AURKA), B (AURKB), and C (AURKC) are potential therapeutic targets in proliferating cells. However, their role has not been clarified in microglia. The aim of this study was to examine the regulation of aurora kinases and their roles and druggability in spinal microgliosis and neuropathic pain. Sprague-Dawley rats received chronic constriction injury (CCI). Gene expression of aurora kinases A-C was evaluated by quantitative RT-PCR and western blot, respectively, in spinal cords at 1, 3, 7, and 14 days after CCI. AURKB gene and protein expression was up-regulated concomitantly with th…

0301 basic medicineMaleDown-RegulationGene ExpressionMicrogliosisBiochemistryRats Sprague-Dawley03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicinePeripheral Nerve InjuriesMedicineAnimalsAurora Kinase BAURKB GeneEnzyme InhibitorsGene knockdownMicrogliabusiness.industryKinaseSpinal cordRatsDisease Models Animal030104 developmental biologymedicine.anatomical_structureSpinal CordGene Knockdown TechniquesPeripheral nerve injuryNeuropathic painCancer researchNeuralgiaMicrogliabusiness030217 neurology & neurosurgeryJournal of neurochemistryReferences
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2-Methoxyestradiol confers neuroprotection and inhibits a maladaptive HIF-1α response after traumatic brain injury in mice

2014

HIF-1α is pivotal for cellular homeostasis in response to cerebral ischemia. Pharmacological inhibition of HIF-1α may reduce secondary brain damage by targeting post-translational mechanisms associated with its proteasomal degradation and nuclear translocation. This study examined the neuroprotective effects of 2-methoxyestradiol (2ME2), the involved HIF-1α-dependent response, and alternative splicing in exon 14 of HIF-1α (HIF-1α∆Ex14) after traumatic brain injury (TBI) in mice. Intraperitoneal 2ME2 administration 30 min after TBI caused a dose-dependent reduction in secondary brain damage after 24 h. 2ME2 was physiologically tolerated, showed no effects on immune cell brain migration, and …

MaleTraumatic brain injuryBlotting WesternIschemiaCellular homeostasisBrain damagePharmacologyBiologyBiochemistryNeuroprotectionBrain IschemiaMitochondrial ProteinsMiceCellular and Molecular Neurosciencechemistry.chemical_compoundPlasminogen Activator Inhibitor 1medicineAnimalsCell NucleusNeuronsEstradiolTumor Necrosis Factor-alphaAlternative splicingMembrane ProteinsExonsHypoxia-Inducible Factor 1 alpha Subunitmedicine.diseaseImmunohistochemistryUp-RegulationMice Inbred C57BLAlternative SplicingProtein TransportNeuroprotective AgentsGene Expression RegulationchemistryBrain InjuriesPlasminogen activator inhibitor-1Tumor necrosis factor alphamedicine.symptomNeuroscienceInjections IntraperitonealSubcellular FractionsJournal of Neurochemistry
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