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Updated: Jan 21, 2026

Quantification of Atherosclerosis in Mice
Published on: June 12, 2019
Data showing atherosclerosis-associated differentially methylated regions are often at enhancers
Michelle Lacey1,2, Carl Baribault1, Kenneth C Ehrlich3
1Tulane Cancer Center, Tulane University Health Sciences Center, LA 70112, USA.
Abstract:
Atherosclerosis involves phenotypic modulation and transdifferentiation of vascular smooth muscle cells (SMCs). Data are given in tabular or figure format that illustrate genome-wide DNA methylation alterations in atherosclerotic vs. control aorta (athero DMRs). Data based upon publicly available chromatin state profiles are also shown for normal aorta, monocyte, and skeletal muscle tissue-specific DMRs and for aorta-specific chromatin features (enhancer chromatin, promoter chromatin, repressed chromatin, actively transcribed chromatin). Athero hypomethylated and hypermethylated DMRs as well as epigenetic and transcription profiles are described for the following genes: ACTA2, MYH10, MYH11 (SMC-associated genes); SMAD3 (a signaling gene for SMCs and other cell types); CD79B and SH3BP2 (leukocyte-associated genes); and TBX20 and genes in the HOXA, HOXB, HOXC, and HOXD clusters (T-box and homeobox developmental genes). The data reveal strong correlations between athero hypermethylated DMRs and regions of enhancer chromatin in aorta, which are discussed in the linked research article "Atherosclerosis-associated differentially methylated regions can reflect the disease phenotype and are often at enhancers" (M. Lacey et al., 2019).
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