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. 2010 Sep 9;89(2):446–456. doi: 10.1093/cvr/cvq291

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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2010. For permissions please email: journals.permissions@oxfordjournals.org.

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Increase in histone acetylation (H3K9/14) and methylation (H3K4) on Smad2 promoter. (A) Increased acetylated and methylated lysine staining (red) is observed in aneurysmal SMCs and colocalizes with H1 histone staining (green) in the nucleus. Scale bar: 50 µm. (B–D) ChIP performed with aneurysmal and control media (B and C) or adventitia (D). After ChIP, PCR is performed with primers annealing specific sequences upstream to 1a TSS (B and D) or 1b TSS (C). Representative migrations of immunoprecipitated (IP) and non-immunoprecipitated (INPUT) samples are shown for each precipitation. An increase in H3K9/14ac and H3K4me is observed upstream to the 1a TSS, only in aneurysmal SMCs (all aetiologies included, no difference between aetiologies). Results are expressed as %IP/INPUT. *Significant increase in H3K9/14ac (TAA: 36.4 ± 13.3 vs. control: 13.6 ± 1.9; P < 0.01) and H3K4me (TAA: 14.7 ± 10.5 vs. control: 1.8 ± 1.6; P < 0.05) is observed in TAA (all aetiologies included) compared with control.