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Vascular smooth muscle cell state trajectories mediate molecular mechanisms of coronary disease risk [ChIP-seq]

GSE316713 Homo sapiens Genome binding/occupancy profiling by high throughput sequencing 3 samples Submitted 2026/02/25 Platform GPL11154Platform GPL24676
Summary
To investigate the genetic basis of SMC cell state trajectories that underlie the SMC component of CAD causality, we developed a dense timecourse single cell transcriptomic and epigenomic mapping of atherosclerosis in a murine disease model with additional high throughput spatial RNA in situ hybridization to localize . We further performed parallel knockout studies with single cell transcriptomics and epigenomics of validated CAD gene Tcf21 to understand its molecular mechanisms in SMC transition. We identified TEAD1 and CEBPB to share significant binding sites with coronary artery disease risk gene TCF21 at enhancer sites across the genome and characterize their genomic relationships through a combination of chromatin immunoprecipitation sequencing for TEAD1, CEBPB, and marker of enhancer activation H3K27ac. We further perform bulk RNAseq to understand the functional effects of TEAD1 knockdown in immortalized smooth muscle cells.
Published in
Vascular smooth muscle cell state trajectories mediate molecular mechanisms of coronary disease risk
Li DY, Kundu S, Cheng P et al. · Nature communications 2026 · PMID 41844614 · doi:10.1038/s41467-026-70530-z
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Also filed as BioProject PRJNA1403812 and SRA study SRP663443. Searching any of these in the dataset finder brings you back here.

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