Related Experiment Video
Updated: Jul 11, 2025
Preparation of a Non-Cardiomyocyte Cell Suspension for Single-Cell RNA Sequencing from a Post-Myocardial Infarction Adult Mouse Heart
Published on: February 3, 2023
Novel Targets Regulating the Role of Endothelial Cells and Angiogenesis after Infarction: A RNA Sequencing Analysis
María Ortega1, Tamara Molina-García1, Jose Gavara2
1INCLIVA Biomedical Research Institute, 46010 Valencia, Spain.
Insights
This study reveals key genes influencing endothelial cell (EC) behavior after heart attack (myocardial infarction). It identifies distinct gene patterns for EC proliferation, apoptosis, and blood vessel formation, crucial for cardiac repair.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Genomics
Background:
- Endothelial cells (ECs) are vital for maintaining heart function and microvasculature after myocardial infarction (MI).
- Understanding gene expression changes in ECs post-MI is crucial for developing cardioprotective strategies.
Purpose of the Study:
- To identify genes regulating endothelial cell proliferation, apoptosis, and angiogenesis following myocardial infarction using RNA-sequencing data.
- To elucidate the temporal dynamics of these processes in the post-MI cardiac environment.
Main Methods:
- Analysis of publicly available RNA-sequencing datasets from eight studies (92 mice) involving coronary ischemia or sham procedures.
- Functional enrichment analysis using gene ontology biological processes (BPs) to identify key pathways and genes.
Main Results:
- Apoptosis-related gene pathways are activated early (up to day 3), while endothelial proliferation genes become overrepresented from day 3 onwards (37 genes).
- Endothelial apoptosis involves both extrinsic (13 genes) and intrinsic (2 genes) signaling pathways.
- Pro-angiogenic pathways are upregulated early post-ischemia, with anti-angiogenic mechanisms appearing by day 3; 51 pro-angiogenic and 29 anti-angiogenic factors showed altered expression.
Conclusions:
- This study provides the first comprehensive RNA-sequencing based evaluation of genes involved in post-MI endothelial cell physiology and angiogenesis.
- The identified genes and pathways offer novel insights into endothelial cell responses after MI, potentially guiding future therapeutic interventions for cardiac repair.
Abstract:
Endothelial cells (ECs) are a key target for cardioprotection due to their role in preserving cardiac microvasculature and homeostasis after myocardial infarction (MI). Our goal is to identify the genes involved in post-MI EC proliferation, EC apoptosis, and angiogenesis regulation via RNA-sequencing transcriptomic datasets. Using eight studies from the Gene Expression Omnibus, RNA-sequencing data from 92 mice submitted to different times of coronary ischemia or sham were chosen. Functional enrichment analysis was performed based on gene ontology biological processes (BPs). Apoptosis-related BPs are activated up to day 3 after ischemia onset, whereas endothelial proliferation occurs from day 3 onwards, including an overrepresentation of up to 37 genes. Endothelial apoptosis post-MI is triggered via both the extrinsic and intrinsic signaling pathways, as reflected by the overrepresentation of 13 and 2 specific genes, respectively. BPs implicated in new vessel formation are upregulated soon after ischemia onset, whilst the mechanisms aiming at angiogenesis repression can be detected at day 3. Overall, 51 pro-angiogenic and 29 anti-angiogenic factors displayed altered transcriptomic expression post-MI. This is the first study using RNA sequencing datasets to evaluate the genes participating in post-MI endothelium physiology and angiogenesis regulation. These novel data could lay the groundwork to advance understanding of the implication of ECs after MI.
Related Concept Videos
01:24Regulation of Angiogenesis and Blood Supply
01:10Mechanism of Angiogenesis