Search results for " neuronal apoptosis"

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Membrane vesicles shed by oligodendroglioma cells induce neuronal apoptosis.

2006

In order to investigate the mechanism by which oligodendrogliomas cause neuronal damage, media conditioned by G26/24 oligodendroglioma cells, were fractionated into shed vesicles and vesicle-free supernatants, and added to primary cultures of rat fetal cortical neurons. After one night treatment with vesicles, a reproducible, dose-dependent, inhibitory effect on neurite outgrowth was already induced and, after 48-72 h of incubation, neuronal apoptosis was evident. Vesicle-free supernatants and vesicles shed by NIH-3T3 cells had no inhibitory effects on neurons. Western blot analyses showed that treated neurons expressed a decreased amount of neurofilament (NF), growth-associated protein (GA…

Cancer ResearchCell signalingProgrammed cell deathPathologymedicine.medical_specialtyNeurofilamentFas Ligand ProteinNeuriteCellOligodendrogliomaApoptosisCell CommunicationBiologyRats Sprague-DawleyMiceWestern blotmedicineAnimalsMyelin SheathCerebral CortexNeuronsmedicine.diagnostic_testVesicleCytoplasmic Vesiclesoligodendroglioma membrane vesicles neuronal apoptosis Fas-L Nogo.Cell biologyRatsmedicine.anatomical_structureOncologyNIH 3T3 CellsNeuronInternational journal of oncology
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The Role of Erythropoietin in Neuroprotection: Therapeutic Perspectives

2007

Nervous system diseases are very complex conditions comprising a large variety of local and systemic responses. Several therapeutic agents interfering with all or in part the biochemical steps that ultimately cause neuronal death have been demonstrated to be neuroprotective in preclinical models. However, all the agents so far investigated have inexorably failed in the phase III trials carried out. A large body of evidence suggests that the hormone erythropoietin (EPO), besides its well-known hematopoietic action, exerts beneficial effects in the central nervous system. EPO's effect has been assessed in several experimental models of brain and spinal cord injury thus becoming a serious cand…

Nervous systemEXPERIMENTAL SUBARACHNOID HEMORRHAGECentral nervous systemSIGNAL-TRANSDUCTIONPharmacologyModels BiologicalNeuroprotectionErythropoietin in neuroprotectionNEURONAL APOPTOSISCEREBROSPINAL-FLUIDAnimalsHumansMedicineIN-VIVO EVIDENCEErythropoietinSpinal cord injuryPharmacologyCEREBRAL-ISCHEMIACOMMON BETA-SUBUNITbusiness.industryRECOMBINANT-HUMAN-ERYTHROPOIETIN; GLYCOGEN-SYNTHASE KINASE-3-BETA; EXPERIMENTAL SUBARACHNOID HEMORRHAGE; COMMON BETA-SUBUNIT; IN-VIVO EVIDENCE; CEREBRAL-ISCHEMIA; SIGNAL-TRANSDUCTION; CEREBROSPINAL-FLUID; NEURONAL APOPTOSIS; CYTOKINE RECEPTORSRECOMBINANT-HUMAN-ERYTHROPOIETINmedicine.diseaseRecombinant ProteinsEnzyme ActivationStrokeClinical trialNeuroprotective AgentsTreatment Outcomemedicine.anatomical_structureErythropoietinGLYCOGEN-SYNTHASE KINASE-3-BETACYTOKINE RECEPTORSBone marrowMitogen-Activated Protein Kinasesbusinessmedicine.drugDrug News & Perspectives
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