0000000000180140

AUTHOR

Regina Hummel

showing 9 related works from this author

Depletion of regulatory T cells increases T cell brain infiltration, reactive astrogliosis, and interferon-γ gene expression in acute experimental tr…

2019

Abstract Background Traumatic brain injury (TBI) is a major cause of death and disability. T cells were shown to infiltrate the brain during the first days after injury and to exacerbate tissue damage. The objective of this study was to investigate the hitherto unresolved role of immunosuppressive, regulatory T cells (Tregs) in experimental TBI. Methods “Depletion of regulatory T cell” (DEREG) and wild type (WT) C57Bl/6 mice, treated with diphtheria toxin (DTx) to deplete Tregs or to serve as control, were subjected to the controlled cortical impact (CCI) model of TBI. Neurological and motor deficits were examined until 5 days post-injury (dpi). At the 5 dpi endpoint, (immuno-) histological…

0301 basic medicinePathologymedicine.medical_specialtyTraumatic brain injuryRegulatory T cellT cellImmunologyT cellsExcitotoxicityBrain damagemedicine.disease_causelcsh:RC346-42903 medical and health sciencesCellular and Molecular NeuroscienceTraumatic brain injury0302 clinical medicinemedicineImmune responselcsh:Neurology. Diseases of the nervous systemInflammationGlial fibrillary acidic proteinbiologybusiness.industryResearchGeneral Neurosciencemedicine.diseaseAstrogliosisCD8A030104 developmental biologymedicine.anatomical_structureNeurologyAstrocytesbiology.proteinCytokinesMicrogliamedicine.symptombusiness030217 neurology & neurosurgeryJournal of Neuroinflammation
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Correction to: Depletion of regulatory T cells increases T cell brain infiltration, reactive astrogliosis, and interferon-γ gene expression in acute …

2019

Traumatic brain injury (TBI) is a major cause of death and disability. T cells were shown to infiltrate the brain during the first days after injury and to exacerbate tissue damage. The objective of this study was to investigate the hitherto unresolved role of immunosuppressive, regulatory T cells (Tregs) in experimental TBI."Depletion of regulatory T cell" (DEREG) and wild type (WT) C57Bl/6 mice, treated with diphtheria toxin (DTx) to deplete Tregs or to serve as control, were subjected to the controlled cortical impact (CCI) model of TBI. Neurological and motor deficits were examined until 5 days post-injury (dpi). At the 5 dpi endpoint, (immuno-) histological, protein, and gene expressio…

InflammationGeneral NeuroscienceImmunologyCorrectionBrainT-Lymphocytes Regulatorylcsh:RC346-429Lymphocyte DepletionCellular and Molecular NeuroscienceDisease Models AnimalInterferon-gammaMiceNeurologyAstrocytesBrain Injuries TraumaticAnimalsGliosislcsh:Neurology. Diseases of the nervous systemJournal of Neuroinflammation
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Administration of all‐ trans retinoic acid after experimental traumatic brain injury is brain protective

2020

BACKGROUND AND PURPOSE: All‐trans retinoic acid (ATRA) is a vitamin A metabolite, important in the developing and mature brain. Pre‐injury ATRA administration ameliorates ischaemic brain insults in rodents. This study examined the effects of post‐traumatic ATRA treatment in experimental traumatic brain injury (TBI). EXPERIMENTAL APPROACH: Male adult mice were subjected to the controlled cortical impact model of TBI or sham procedure and killed at 7 or 30 days post‐injury (dpi). ATRA (10 mg kg−1, i.p.) was given immediately after the injury and 1, 2 and 3 dpi. Neurological function and sensorimotor coordination were evaluated. Brains were processed for (immuno‐) histological, mRNA and protei…

Male0301 basic medicineTraumatic brain injuryRetinoic acidTretinoinPharmacologyHippocampal formationHMGB1Mice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineBrain Injuries TraumaticmedicineAnimalsInflammationPharmacologyMicrogliabiologybusiness.industryBrainmedicine.diseaseGranule cellResearch PapersAstrogliosis030104 developmental biologymedicine.anatomical_structurechemistryBlood-Brain BarrierApoptosisbiology.proteinbusiness030217 neurology & neurosurgeryBritish Journal of Pharmacology
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Progranulin protects against exaggerated axonal injury and astrogliosis following traumatic brain injury

2016

In response to traumatic brain injury (TBI) microglia/macrophages and astrocytes release inflammatory mediators with dual effects on secondary brain damage progression. The neurotrophic and anti-inflammatory glycoprotein progranulin (PGRN) attenuates neuronal damage and microglia/macrophage activation in brain injury but mechanisms are still elusive. Here, we studied histopathology, neurology and gene expression of inflammatory markers in PGRN-deficient mice (Grn-/- ) 24 h and 5 days after experimental TBI. Grn-/- mice displayed increased perilesional axonal injury even though the overall brain tissue loss and neurological consequences were similar to wild-type mice. Brain inflammation was …

0301 basic medicinePathologymedicine.medical_specialtyTraumatic brain injuryInflammationBrain damageBlood–brain barrier03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicinemedicineNeuroinflammationMicrogliabiologybusiness.industrymedicine.diseaseAstrogliosis030104 developmental biologymedicine.anatomical_structurenervous systemNeurologybiology.proteinmedicine.symptombusiness030217 neurology & neurosurgeryNeurotrophinGlia
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Ferroelectricity and piezoelectricity in soft biological tissue: Porcine aortic walls revisited

2017

Recently reported piezoresponse force microscopy (PFM) measurements have proposed that porcine aortic walls are ferroelectric. This finding may have great implications for understanding biophysical properties of cardiovascular diseases such as arteriosclerosis. However, the complex anatomical structure of the aortic wall with different extracellular matrices appears unlikely to be ferroelectric. The reason is that a prerequisite for ferroelectricity, which is the spontaneous switching of the polarization, is a polar crystal structure of the material. Although the PFM measurements were performed locally, the phase-voltage hysteresis loops could be reproduced at different positions on the tis…

PermittivityMaterials sciencePhysics and Astronomy (miscellaneous)FerroelectricityPiezoresponse force microscopyPiezoelectricityHOL - HolstNanotechnology02 engineering and technologyDielectricPFM01 natural sciences0103 physical sciences010306 general physicsTS - Technical SciencesIndustrial InnovationElectrostrictionCondensed matter physics021001 nanoscience & nanotechnologyPiezoelectricityFerroelectricityHysteresisPorcine aortic wallsPiezoresponse force microscopyNano Technology0210 nano-technologyElectric displacement fieldBiological tissue
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Plasminogen activator inhibitor‐1 augments damage by impairing fibrinolysis after traumatic brain injury

2019

Objective Plasminogen activator inhibitor-1 (PAI-1) is the key endogenous inhibitor of fibrinolysis, and enhances clot formation after injury. In traumatic brain injury, dysregulation of fibrinolysis may lead to sustained microthrombosis and accelerated lesion expansion. In the present study, we hypothesized that PAI-1 mediates post-traumatic malfunction of coagulation, with inhibition or genetic depletion of PAI-1 attenuating clot formation and lesion expansion after brain trauma. Methods We evaluated PAI-1 as a possible new target in a mouse controlled cortical impact (CCI) model of traumatic brain injury. We performed the pharmacological inhibition of PAI-1 with PAI-039 and stimulation b…

Male0301 basic medicineTraumatic brain injurymedicine.medical_treatmentBrain damagePharmacologyLesionMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineBrain Injuries TraumaticSerpin E2FibrinolysisAnimalsMedicineThrombusResearch ArticlesIndoleacetic Acidsbusiness.industryFibrinolysisBrainmedicine.diseaseMice Inbred C57BL030104 developmental biologyNeurologychemistryPlasminogen activator inhibitor-1Neurology (clinical)medicine.symptombusinessPlasminogen activator030217 neurology & neurosurgeryIntravital microscopyResearch ArticleAnnals of Neurology
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Pharmacologic Inhibition of ADAM10 Attenuates Brain Tissue Loss, Axonal Injury and Pro-inflammatory Gene Expression Following Traumatic Brain Injury …

2021

The α-secretase A disintegrin and metalloprotease 10 (ADAM10) regulates various physiological and pathophysiological processes. Despite its broad functional implications during development, plasticity, and disease, no pharmacological approaches to inhibit ADAM10 in acute brain injury have been reported. Here, we examined the effects of the ADAM10 inhibitor GI254023X on the neurological and histopathological outcome after experimental traumatic brain injury (TBI). C57BL/6N mice were subjected to the controlled cortical impact (CCI) model of TBI or sham procedure and received GI254023X or vehicle during the acute phase of injury (n = 40, 100 mg/kg, 25% DMSO, 0.1 M Na2CO3, intraperitoneal, 30 …

Traumatic brain injuryADAM10PharmacologyBlood–brain barrierNeuroprotectionneuroinflammationaxonal injuryCell and Developmental Biologymedicinelcsh:QH301-705.5NeuroinflammationOriginal ResearchMicrogliabiologybusiness.industrytraumatic brain injuryADAM10 (a disintegrin and metalloprotease 10)Glutamate receptorCell Biologymedicine.diseaseGI254023Xmedicine.anatomical_structurelcsh:Biology (General)biology.proteinneuroprotectionGRIN2BbusinessDevelopmental BiologyFrontiers in Cell and Developmental Biology
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Effect of fluid resuscitation on cerebral integrity: A prospective randomised porcine study of haemorrhagic shock.

2021

BACKGROUND The treatment of haemorrhagic shock is a challenging task. Colloids have been regarded as standard treatment, but their safety and benefit have been the subject of controversial debates. Negative effects, including renal failure and increased mortality, have resulted in restrictions on their administration. The cerebral effects of different infusion regimens are largely unknown. OBJECTIVES The current study investigated the impact of gelatine-polysuccinate, hydroxyethyl starch (HES) and balanced electrolyte solution (BES) on cerebral integrity, focusing on cerebral inflammation, apoptosis and blood flow in pigs. DESIGN Randomised experimental study. SETTING University-affiliated …

Resuscitationbusiness.industrySwineResuscitationHemodynamicsBlood flowHydroxyethyl starchShock HemorrhagicMicrocirculationHydroxyethyl Starch DerivativesAnesthesiology and Pain MedicineShock (circulatory)AnesthesiamedicineArterial bloodAnimalsFluid TherapyProspective Studiesmedicine.symptomCerebral perfusion pressurebusinessmedicine.drugEuropean journal of anaesthesiology
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Single intracerebroventricular progranulin injection adversely affects the blood–brain barrier in experimental traumatic brain injury

2021

Progranulin (PGRN) is a neurotrophic and anti-inflammatory factor with protective effects in animal models of ischemic stroke, subarachnoid hemorrhage, and traumatic brain injury (TBI). Administration of recombinant (r) PGRN prevents exaggerated brain pathology after TBI in Grn-deficient mice, suggesting that local injection of recombinant progranulin (rPGRN) provides therapeutic benefit in the acute phase of TBI. To test this hypothesis, we subjected adult male C57Bl/6N mice to the controlled cortical impact model of TBI, administered a single dose of rPGRN intracerebroventricularly (ICV) shortly before the injury, and examined behavioral and biological effects up to 5 days post injury (dp…

Male0301 basic medicinemedicine.medical_specialtySubarachnoid hemorrhageTraumatic brain injuryPrimary Cell Culture610 MedizinBlood–brain barrierOccludinBiochemistryNeuroprotectionMice03 medical and health sciencesCellular and Molecular NeuroscienceProgranulins0302 clinical medicineInternal medicine610 Medical sciencesBrain Injuries TraumaticmedicineAnimalsNeuroinflammationInjections IntraventricularTight Junction ProteinsBehavior AnimalMicrogliabiologybusiness.industrymedicine.diseaseRecombinant ProteinsMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureEndocrinologyAnimals NewbornBlood-Brain BarrierAstrocytesbiology.proteinEncephalitisMicrogliabusiness030217 neurology & neurosurgeryNeurotrophin
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