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. 2019 Jan 8;10(6):672–683. doi: 10.1007/s12975-018-0683-2

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© The Author(s) 2019

Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

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Fig. 1 — MiR-212/132 are upregulated after oxygen-glucose deprivation in mouse brain microvascular endothelial cells. MiR-212/132 levels were measured in oxygen-glucose deprivation (OGD)- or OGD/re-oxygenation (OGD/reox)-treated cEND cells (a) and mouse primary brain microvascular endothelial cells (BMEC) (b) by qPCR. Data were normalized to control cells cultured in standard conditions (normox) which was set as 1 and is presented as an average of three independent experiments with standard deviations. c MiR-212/132 levels were measured in mouse cerebral capillaries isolated from mouse brains after traumatic brain injury (TBI) and normalized to expression levels in non-injured hemisphere (control) (n = 6/group), *p < 0.05