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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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CCL5 expression in ascending aorta of humans and mice. (A) Immunohistochemistry of CCL5 in non-diseased artery, advanced plaques, and unstable plaques of human samples. (B) Quantitative analysis of CCL5 expression in (A) (n = 3, *P <0.05, **P <0.01). (C) Immunohistochemistry of CCL5 in non-diseased artery, advanced plaques, and unstable plaques of ApoE^−/− mice. (D) Quantitative analysis of CCL5 expression in (C) (n = 3, *P <0.05, **P <0.01). Bars represent mean ± standard deviation. ApoE, apolipoprotein E; CCL5, chemokine (C-C motif) ligand 5; IPH, thin capped fibroatheroma with intraplaque hemorrhage (advanced unstable plaques); ND, non-diseased arteries; n.s., non-significant; TfcA, thick fibrous cap atheroma (advanced stable plaques).