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. 2020 Dec 17;41(3):1127–1145. doi: 10.1161/ATVBAHA.120.315031

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© 2020 The Authors.

Arteriosclerosis, Thrombosis, and Vascular Biology is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

This article is made available via the PMC Open Access Subset for unrestricted re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the COVID-19 pandemic or until permissions are revoked in writing. Upon expiration of these permissions, PMC is granted a perpetual license to make this article available via PMC and Europe PMC, consistent with existing copyright protections.

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Figure 6. — Extracellular vesicle (EV) administration mitigates middle cerebral artery occlusion (MCAO)-induced upregulation of ABCB1 (ATP-binding cassette subfamily B member 1 transporter) and MMP-9 (matrix metalloproteinase 9) as well as activation of NF-κB (nuclear factor-κB) in ischemic microvessels. Mice were exposed to 60 min of middle cerebral artery (MCA) occlusion followed by 24 h of survival. Sham group mice underwent the surgery procedure without MCA occlusion. Mice were treated with PBS (control and sham) or intravenously treated at the beginning of reperfusion and 6 h later with another EV administration. A, In the schematic diagram, EVs reach endothelial cells (ECs), cross the blood-brain barrier (BBB), enter end-feet of astrocytes, and arrive in the brain parenchyma outside of microvessels. B, EVs labeled with DiI (red) reached ECs of the brain tissue as shown by immunofluorescence staining against CD31 (green). Furthermore, EVs-DiI (red spots) were also detected in the brain parenchyma outside of the microvessels with some positive signaling in astrocytes (GFAP [glial fibrillary acidic protein], green). Scale bars: 20 µm. C and E, Quantitative analysis of ABCB1, p65, and MMP-9 expression in sham, MCAO, and MCAO treated with EVs by Western blot analysis of the hemisphere microvessels. Western blot was normalized with the housekeeping protein α-tubulin or β-actin (n=5 per group). F, Analysis of MMP-9 and MMP-2 activity using gelatin zymography of the ischemic hemisphere or sham hemisphere. G, Quantitative analysis of MMP-9 (red) expression by immunofluorescence staining and measurement of fluorescence intensity of the ischemic striatum in the 3 groups. GFAP (green) represents a specific maker of astrocytes. Scale bars: 50 µm. H, Analysis of the blood-brain barrier integrity using the Evans blue extravasation assay in ischemic hemispheres of the three groups (n=5 per group). Data are expressed as mean±SD, *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001, #P<0.05 and ##P<0.001.