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Changes in components of the brain extracellular matrix after experimental ischemic stroke

datacite.subject.fosCiências Médicas::Biotecnologia Médicapt_PT
dc.contributor.advisorWieloch, Tadeusz
dc.contributor.advisorAraújo, Inês
dc.contributor.advisorQuattromani, Miriana Jlenia
dc.contributor.authorGuerreiro, Carla Sofia de Jesus
dc.date.accessioned2016-04-12T10:19:08Z
dc.date.available2016-04-12T10:19:08Z
dc.date.issued2014
dc.date.submitted2014
dc.descriptionDissertação de mestrado, Ciências Biomédicas, Departamento de Ciências Biomédicas e Medicina , Universidade do Algarve; Laboratory for Experimental Brain Research, Lund University, 2014
dc.description.abstractStroke is the 3rd cause of death in the world. During stroke, there is a disruption in the blood supply to the brain leading to rapid loss of brain function. Ischemic strokes are caused by obstruction of the blood supply, while hemorrhagic strokes results from rupture of a blood vessel. Eight-five percent of the strokes are ischemic. The only treatment recommended for acute ischemic stroke is the recombinant tissue activator of plasminogen but only a few percentages of patients are eligible for rtPA administration. Approximately 30% of the ischemic stroke victims die and 30% become severely disabled, resulting in among others deficits in motor function in the contralateral musculature. Spontaneous recovery occurs during weeks to months following injury. There are many physiological and anatomical examples of cortical brain plasticity and one of the most potent modulators of cortical structure and function is behavioral experience. Functional recovery after stroke can be enhanced by physical training in stroke patients. In the animal settings, physical training can be accomplished by enriched environment (EE). EE refers to housing conditions, either home cages or exploratory chamber, that facilitate enhanced sensory, cognitive and motor stimulation relative to standard housing conditions. The extracellular matrix (ECM) is important in the regulation of brain plasticity but is also a potential hampering factor for recovery after stroke. It is known that EE affects chondroitin sulfate proteoglycans (CSPGs) present in ECM, leading to functional recovery. Matrix metalloproteinases (MMPs) are able to cleave ECM components. There are some evidences that beta-dystroglycan (β-DG) is a MMP-9 target. After the degradation of β-DG, there is a 30 kDa product. The aim of this work is to explore how EE affects β-DG and gelatinases over 1 week of recovery after experimental stroke, performed as photothrombosis (PT). We show that EE does not affect the infarct size and improves tactile/proprioceptive response to limb stimulation. We found that β-DG is mostly present in vessels across the brain cortex and animals housed in an EE had a higher degradation than STD animals when comparing to sham non-operated animals. β-DG can be related with changes in the ECM that leads to brain plasticity, promoting functional recovery after experimental stroke, possibly due to MMPs enzymatic activity.pt_PT
dc.identifier.tid202213200
dc.identifier.urihttp://hdl.handle.net/10400.1/7977
dc.language.isoengpt_PT
dc.subjectCiências biomédicaspt_PT
dc.subjectAVCpt_PT
dc.subjectEnfarte do miocárdiopt_PT
dc.subjectTrombosept_PT
dc.subjectTerapiaspt_PT
dc.titleChanges in components of the brain extracellular matrix after experimental ischemic strokept_PT
dc.typemaster thesis
dspace.entity.typePublication
rcaap.rightsopenAccesspt_PT
rcaap.typemasterThesispt_PT
thesis.degree.grantorUniversidade do Algarve. Departamento de Ciências Biomédicas e Medicina
thesis.degree.grantorLund University. Laboratory for Experimental Brain Research
thesis.degree.levelMestre
thesis.degree.nameMestrado em Ciências Biomédicaspt_PT

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