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. Author manuscript; available in PMC: 2014 Sep 13.
Published in final edited form as: Circ Res. 2013 Sep 13;113(7):10.1161/CIRCRESAHA.113.302138. doi: 10.1161/CIRCRESAHA.113.302138

Figure 1.

Figure 1

Vascular smooth muscle cells (VSMCs) from thoracic aortic aneurysm (TAA) switch from a Myc-dependent repression to a p53- and histone acetylation-dependent activation of the SMAD2 promoter. Top: In normal VSMCs, Myc binding prevents transcription of the SMAD2 locus and the nearby chromatin is quite compact. Bottom: In TAA VSMCs, Myc is displaced and p53 binding and histone acetylation of the promoter driven by p300 and PCAF, two histone acetyltransferases, leads to chromatin relaxation and activates transcription of SMAD2. Nucleosomes are schemactically represented as cyclinders wrapped with DNA.