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. 2015 Mar 19;6(1):36. doi: 10.1186/s13287-015-0026-0

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© Zhang et al.; licensee BioMed Central. 2015

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Overexpression of CCR5 in endothelial progenitor cells (EPCs) promoted the recruitment of EPCs into atherosclerotic plaques. (A) Representative images of EPC incorporation on atherosclerotic plaques 6 weeks after phosphate-buffered saline (PBS), EPC (Lenti-EGFP), and CCR5 overexpression of EPC treatment (Lenti-CCR5). DAPI (blue), EGFP (green), CD31 (red). Arrowheads indicate EPCs (EGFP⁺). (B) Quantitative analysis of migrated EPCs on atherosclerotic plaques in Lenti-EGFP and Lenti-CCR5 groups (*P <0.05, **P <0.01). The average number of EGFP⁺ EPCs on atherosclerotic plaques was counted from three randomly chosen high-power fields (magnification, 200×). Bars represent mean ± standard deviation. CCR5, chemokine (C-C motif) receptor 5; DAPI, 4′, 6-diamidino-2-phenylindole; EGFP, enhanced green fluorescent protein.