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. 2019 Nov 14;9:16819. doi: 10.1038/s41598-019-53418-5

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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The migration of administrated OGD-PBMCs. (A) Administrated OGD-PBMCs from GFP mice (green, OGD-GFP-PBMCs) migrated into the border area between the ischemic core and the penumbra at 3 days after administration in triplicates. However, signals were not observed in the brain samples from administration of normoxic PBMCs from GFP mice (normoxic GFP-PBMCs). Scale bar, 50 μm. Analyses with 4′, 6′-diamidino-2-phenylindole (DAPI; blue) were performed by an investigator blinded to the therapeutic information. (B) Representative western blotting and bar graphs showing the relative signal intensities of monocyte chemoattractant protein-1 (MCP-1) from the conditioned media of rat primary-cultured PBMCs subjected to either normoxia (norm) or OGD (N = 5 each). The increase in the level of MCP-1 reveals that OGD-PBMCs might migrate in response to MCP-1 into the brain parenchyma. Transferrin confirmed an equal loading of proteins. Data represent relative optical densities of each sample compared to the loading control band by unpaired t-test. ^**P < 0.01 (N = 5).