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Publication
Changes in components of the brain extracellular matrix after experimental ischemic stroke
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Authors
Abstract(s)
Stroke 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.
Description
Dissertação de mestrado, Ciências Biomédicas, Departamento de Ciências Biomédicas e Medicina , Universidade do Algarve; Laboratory for Experimental Brain Research, Lund University, 2014
Keywords
Ciências biomédicas AVC Enfarte do miocárdio Trombose Terapias