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Updated: Jul 2, 2026
Isolation and Profiling of Human Primary Mesenteric Arterial Endothelial Cells at the Transcriptome Level
Published on: March 14, 2022
In vivo differences between endothelial transcriptional profiles of coronary and iliac arteries revealed by
Ji Zhang1, Kelley A Burridge, Morton H Friedman
1Department of Biomedical Engineering, Duke University, Durham, North Carolina 27708, USA.
Insights
Coronary artery endothelial cells (ECs) show distinct gene expression compared to iliac artery ECs, revealing molecular differences that may explain why coronary arteries are more prone to atherosclerosis.
Area of Science:
- Vascular Biology and Atherosclerosis Research
- Genomics and Transcriptomics
- Cellular and Molecular Medicine
Background:
- Endothelial cells (ECs) exhibit significant heterogeneity across different vascular beds.
- This phenotypic heterogeneity is crucial for understanding arterial diseases like atherosclerosis, which disproportionately affects major arteries.
- Arteries vary in their susceptibility to atherosclerosis, suggesting underlying differences in their ECs.
Purpose of the Study:
- To investigate the gene expression differences between endothelial cells from atheroprone coronary arteries and atheroresistant iliac arteries.
- To identify specific genes and pathways involved in the differential atherosusceptibility of these arterial beds.
Main Methods:
- DNA microarrays were employed to compare gene expression profiles of porcine coronary artery endothelial cells (CECs) and iliac artery endothelial cells (IECs).
- Statistical analysis identified differentially expressed genes, with a focus on those related to atherogenesis.
- Quantitative polymerase chain reaction (PCR) was used to validate the expression levels of selected genes (e.g., HOXA10, HOXA9).
Main Results:
- 51 genes were found to be differentially expressed between CECs and IECs.
- Seventeen of these genes are known to be involved in atherogenesis, with atherogenic genes upregulated and atheroprotective genes downregulated in CECs.
- Gene ontology and pathway analysis revealed significant upregulation of genes in CECs related to immune activation, inflammatory responses, and system development.
Conclusions:
- Significant transcriptional differences exist between CECs and IECs.
- These differences, particularly the overexpression of atherogenic genes and inflammatory pathways in CECs, may underlie the higher susceptibility of coronary arteries to atherosclerosis.
- The findings provide novel insights into the molecular mechanisms driving coronary artery atherosusceptibility.
Abstract:
Endothelial cells (ECs) from different vascular beds display a remarkable heterogeneity in both structure and function. Phenotypic heterogeneity among arterial ECs is particularly relevant to atherosclerosis since the disease occurs predominantly in major arteries, which vary in their atherosusceptibility. To explore EC heterogeneity between typical atheroprone and atheroresistant arteries, we used DNA microarrays to compare gene expression profiles of freshly harvested porcine coronary (CECs) and iliac artery (IECs) ECs. Statistical analysis revealed 51 genes that were differentially expressed in CECs relative to IECs at a false discovery rate of 5%. Seventeen of these genes are known to be involved in atherogenesis. Consistent with coronary arteries being more atherosusceptible, almost all putative atherogenic genes were overexpressed in CECs, whereas all atheroprotective genes were downregulated, relative to IECs. A subset of the identified genes was validated by quantitative polymerase chain reaction (PCR). PCR results suggest that the differences in expression levels between CECs and IECs for the HOXA10 and HOXA9 genes were >100-fold. Gene ontology (GO) and biological pathway analysis revealed a global expression difference between CECs and IECs. Genes in twelve GO categories, including complement immune activation, immunoglobulin-mediated response, and system development, were significantly upregulated in CECs. CECs also overexpressed genes involved in several inflammatory pathways, including the classical pathway of complement activation and the IGF-1-mediated pathway. The in vivo transcriptional differences between CECs and IECs found in this study may provide new insights into the factors responsible for coronary artery atherosusceptibility.
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