Atlas of cardiac endothelial cell enhancer elements linking the mineralocorticoid receptor to pathological gene expression.
Lisa DengLuisa PollmeierRebecca BednarzCan CaoPatrick LauretteLuisa WirthArgen MamazhakypovChristine BodeLutz HeinRalf GilsbachAchim LotherPublished in: Science advances (2024)
Endothelial cells play crucial roles in physiology and are increasingly recognized as therapeutic targets in cardiovascular disease. Here, we analyzed the regulatory landscape of cardiac endothelial cells by assessing chromatin accessibility, histone modifications, and 3D chromatin organization and confirmed the functional relevance of enhancer-promoter interactions by CRISPRi-mediated enhancer silencing. We used this dataset to explore mechanisms of transcriptional regulation in cardiovascular disease and compared six different experimental models of heart failure, hypertension, or diabetes. Enhancers that regulate gene expression in diseased endothelial cells were enriched with binding sites for a distinct set of transcription factors, including the mineralocorticoid receptor (MR), a known drug target in heart failure and hypertension. For proof of concept, we applied endothelial cell-specific MR deletion in mice to confirm MR-dependent gene expression and predicted direct MR target genes. Overall, we have compiled here a comprehensive atlas of cardiac endothelial cell enhancer elements that provides insight into the role of transcription factors in cardiovascular disease.
Keyphrases
- endothelial cells
- transcription factor
- gene expression
- cardiovascular disease
- heart failure
- dna methylation
- left ventricular
- high glucose
- contrast enhanced
- genome wide identification
- blood pressure
- binding protein
- dna binding
- type diabetes
- magnetic resonance
- single cell
- genome wide
- vascular endothelial growth factor
- cardiovascular risk factors
- cardiovascular events
- cardiac resynchronization therapy
- magnetic resonance imaging
- emergency department
- atrial fibrillation
- acute heart failure
- coronary artery disease
- dna damage
- glycemic control
- adipose tissue
- adverse drug
- high fat diet induced
- skeletal muscle
- bioinformatics analysis