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J Cereb Blood Flow Metab. 2018 Oct 24:271678X18806893. doi: 10.1177/0271678X18806893. [Epub ahead of print]

Involvement of caveolin-1 in neurovascular unit remodeling after stroke: Effects on neovascularization and astrogliosis.

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1 Department of Clinical Neurosciences, CHUV, Lausanne, Switzerland.
2 Brain Molecular Imaging Lab, CNRS UMR 5287, INCIA, University of Bordeaux, Bordeaux, France.
3 Basic Science Department, Loma Linda University School of Medicine, Loma Linda, CA, USA.


Complex cellular and molecular events occur in the neurovascular unit after stroke, such as blood-brain barrier (BBB) dysfunction and inflammation that contribute to neuronal death, neurological deterioration and mortality. Caveolin-1 (Cav-1) has distinct physiological functions such as caveolae formation associated with endocytosis and transcytosis as well as in signaling pathways. Cav-1 has been proposed to be involved in BBB dysfunction after brain injury; however, its precise role is poorly understood. The goal of this study was to characterize the expression and effect of Cav-1 deletion on outcome in the first week in a transient Middle Cerebral Artery Occlusion stroke model. We found increased Cav-1 expression in new blood vessels in the lesion and in reactive astrocytes in the peri-lesion areas. In Cav-1 KO mice, the lesion volume was larger and the behavioral outcome worse than in WT mice. Cav-1 KO mice exhibited reduced neovascularization and modified astrogliosis, without formation of a proper glial scar around the lesion at three days post injury, coinciding with aggravated outcomes. Altogether, these results point towards a potential protective role of endogenous Cav-1 in the first days after ischemia by promoting neovascularization, astrogliosis and scar formation.


Caveolin-1; astrogliosis; ischemic stroke; neovascularization; neuroprotection


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