Browsing by Author "Guerreiro, Carla Sofia de Jesus"
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- Changes in components of the brain extracellular matrix after experimental ischemic strokePublication . Guerreiro, Carla Sofia de Jesus; Wieloch, Tadeusz; Araújo, Inês; Quattromani, Miriana JleniaStroke 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.