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E u r o S c i C o n C o n f e r e n c e o n
Neurology & Neurological
Disorders
Neurology 2018
J u l y 1 2 - 1 3 , 2 0 1 8
P a r i s , F r a n c e
Page 76
Journal of Neurology and Neuroscience
ISSN: 2171-6625
I
schemic stroke constitute a major cause of death and disability of the adults
in the world. Unfortunately, no efficient therapy does yet exist. Endogenous
neurovascular restorative responses are triggered within the ischemic tissue,
as an attempt from the brain to recover. Ischemic stroke triggers the formation
of new microvasculature in the peri-infarct region via activation of various
angiogenic mechanisms. Neuronal survival is higher in the tissue undergoing
angiogenesis, correlating with longer survival in stroke patients. Angiogenesis
is a highly dynamic process that involves close and finely tuned interactions
between brain endothelial cells and pericytes. Pericytes play major roles in
regulating the cerebral blood flow, angiogenesis, microvasculature stability,
and blood-brain barrier (BBB) properties. Ischemic stroke profoundly affects
the function of pericytes by triggering their death and detachment from brain
endothelial cells, which impairs key neurovascular functionswithin the ischemic
tissue. Using in vivo and in vitro approaches, our recent work demonstrates
that vascular endothelial growth factor isoform-B (VEGF-B), which acts as
survival factor, promotes the formation of stable microvasculature within the
ischemic tissue by specifically enhancing the survival of pericytes and their
interaction with brain endothelial cells. We found that the effects of VEGF-B are
mediated via its specific receptor VEGFR-1 that is predominately expressed
in brain pericytes. Our study unravelled an unknown role of VEGF-B/VEGFR-1
signalling in rescuing the function of pericytes by inducing expression of the
anti-apoptotic protein, B-cell lymphoma 2 (Bcl-2) and AMP-activated protein
kinase α (AMPKα) protein, which is involved in energy homeostasis. Moreover,
VEGF-B/VEGFR-1 signalling stimulates the release of factors stimulating a
reparative angiogenesis that does not compromise microvasculature stability
and BBB permeability. Our findings suggest that strategies aiming to stimulate
the endothelial cell-pericyte crosstalk constitute a promising therapeutic
approach to promote neurovascular repair upon ischemic stroke.
Biography
Ayman ElAli has completed his PhD in 2010 at the University
of Duisburg-Essen in Germany. He pursued his Post-doctoral
trainings at the research centres of University Hospital of Essen
in Germany, and CHU de Québec in Canada. He joined in 2015
the Department of Psychiatry and Neuroscience, Faculty of
Medicine, Laval University, Canada, as an Assistant Professor.
His research program aims at Investigating Neurovascular
Interactions Following Stroke with an Emphasis on Developing
New Therapeutic Approaches. He has published more than 37
papers in top-tier journals and has been serving as Referee in
several reputed funding organizations and journals.
ayman.el-ali@crchudequebec.ulaval.caAyman ElAli, Noemie Jean LeBlanc and Revathy Guruswamy
Research Centre of CHU de Québec -Université Laval, Canada
Ayman ElAli et al., J Neurol Neurosci 2018, Volume: 9
DOI: 10.21767/2171-6625-C1-009
Harnessing the pericytes to promote neurovascular repair
after ischemic stroke