0000000000248379

AUTHOR

Malgorzata Burek

0000-0001-6148-2195

showing 2 related works from this author

Addition of NMDA-receptor antagonist MK801 during oxygen/glucose deprivation moderately attenuates the upregulation of glucose uptake after subsequen…

2011

During stroke the blood–brain barrier (BBB) is damaged which can result in vasogenic brain edema and inflammation. The reduced blood supply leads to decreased delivery of oxygen and glucose to affected areas of the brain. Oxygen and glucose deprivation (OGD) can cause upregulation of glucose uptake of brain endothelial cells. In this letter, we investigated the influence of MK801, a non-competitive inhibitor of the NMDA-receptor, on the regulation of the glucose uptake and of the main glucose transporters glut1 and sglt1 in murine BBB cell line cerebEND during OGD. mRNA expression of glut1 was upregulated 68.7- fold after 6 h OGD, which was significantly reduced by 10 μM MK801 to 28.9-fold.…

medicine.medical_specialtyTime FactorsSchlaganfallNMDA-RezeptorGlucose uptakeNMDA-AntagonistInflammationCarbohydrate metabolismTritiumBlood–brain barrierReceptors N-Methyl-D-AspartateMice03 medical and health sciences0302 clinical medicineDownregulation and upregulationInternal medicinemedicineBlut-Hirn-SchrankeAnimalsddc:610RNA MessengerHypoxia030304 developmental biology0303 health sciencesDose-Response Relationship DrugbiologyGeneral NeuroscienceGlucosetransportproteineGlucose transporterBrainEndothelial CellsUp-RegulationOxygencarbohydrates (lipids)Glucosemedicine.anatomical_structureEndocrinologynervous systembiology.proteinNMDA receptorGLUT1Dizocilpine Maleatemedicine.symptomExcitatory Amino Acid Antagonists030217 neurology & neurosurgeryNeuroscience Letters
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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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