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Biology subjects

de Borst, G. J.

Publications and source records attributed to de Borst, G. J..

7 recordsLinked to original sources

Identification of endothelial-to-mesenchymal transition gene signatures in single-cell transcriptomics of human atherosclerotic tissue

RationaleEndothelial cells can differentiate into mesenchymal-like cells via endothelial to mesenchymal transition (EndoMT). In murine models, cell transitions of EndoMT have been assessed with lineage tracing techniques. Knowledge on molecular mechanisms of EndoMT in human vascular lesions is scarce as studies in human atherosclerosis are limited by observational study designs such as histo-pathological studies. ObjectiveWe aim to identify a human EndoMT gene expression signature by combining experimentally induced in vitro EndoMT with lineage-traced pathways from atherosclerotic mice and extrapolate this to human plaque scRNA-seq data. Methods and resultsFirst, we stimulated human coronary artery endothelial cells (HCAEC) with TNF and TFG{beta} to trigger EndoMT. We executed transcriptomic analyses and defined multiple temporal patterns of gene expression changes during EndoMT. We used Cdh5-CreERT2 Rosa-eYFP apoE-/- lineage traced mouse scRNA-seq data to demonstrate that the temporal in vitro gene expression changes are reflected in EndoMT trajectories in mice plaque tissue. Finally, we constructed three candidate EndoMT lineages across multiple subpopulations of ECs and SMCs in human carotid scRNA-seq data (n=46). We examined gene expression over the course of these lineages and identified 73 markers for the presence of EndoMT such as NRG1 and DEPP1. ConclusionThis study reveals the gene expression profile of EndoMT trajectories in human atherosclerotic plaques by combining RNA-seq data from in vitro models with single-cell transcriptomic datasets. Our gene expression atlas of EndoMT in atherosclerosis could serve as a reference for future studies, providing novel inroads to study atherosclerotic mechanisms for the development of novel therapies.

molecular biology↗

Human primary plaque cell cultures to study mechanisms of atherosclerosis

Plaque smooth muscle cells are critical players in the initiation and advancement of atherosclerotic disease. They produce extracellular matrix (ECM) components, which play a role in lesion progression and stabilization. Despite clear phenotypic differences between plaque smooth muscle cells and vascular smooth muscle cells (VSMCs), VSMCs are still widely used as a model system in atherosclerotic research. Here we present a conditioned outgrowth method to isolate plaque smooth muscle cells. We obtained plaque cells from 27 donors (24 carotid and 3 femoral endarterectomies). We show that these cells keep their proliferative capacity for eight passages, are transcriptionally stable, retain donor-specific gene expression programs, and express extracellular matrix proteins (FN1, COL1A1, DCN) and smooth muscle cell markers (ACTA2, MYH11, CNN1). Single-cell transcriptomics of plaque tissue and cultured cells reveals that cultured plaque cells closely resemble the myofibroblast fraction of plaque smooth muscle cells. Chromatin immunoprecipitation sequencing (ChIP-seq) shows the presence of histone H3 lysine 4 dimethylation (H3K4me2) at the MYH11 promoter, pointing to their smooth muscle cell origin. Finally, we demonstrated that plaque cells can be efficiently transduced (>97%) and are capable to take up oxidized LDL (oxLDL) and undergo calcification. In conclusion, we present a method to isolate and culture primary human plaque cells that retain plaque myofibroblast-like cells phenotypical and functional capabilities - making them a suitable in vitro model for studying selected mechanisms of atherosclerosis.

cell biology↗

Female gene networks are expressed in myofibroblast-like smooth muscle cells in vulnerable atherosclerotic plaques.

Women presenting with coronary artery disease (CAD) more often present with fibrous atherosclerotic plaques, which are currently understudied. Phenotypically modulated smooth muscle cells (SMCs) contribute to atherosclerosis in women. How these phenotypically modulated SMCs shape female versus male plaques is unknown. Here, we show sex-stratified gene regulatory networks (GRNs) from human carotid atherosclerotic tissue. Prioritization of these networks identified two main SMC GRNs in late-stage atherosclerosis. Single-cell RNA-sequencing mapped these GRNs to two SMC phenotypes: a phenotypically modulated myofibroblast-like SMC network and a contractile SMC network. The myofibroblast-like GRN was mostly expressed in plaques that were vulnerable in females. Finally, mice orthologs of the female myofibroblast-like genes showed retained expression in advanced plaques from female mice but were downregulated in male mice during atherosclerosis progression. Female atherosclerosis is driven by GRNs that promote a fibrous vulnerable plaque rich in myofibroblast-like SMCs.

bioinformatics↗

Sex-dependent gene regulation of human atherosclerotic plaques by DNA methylation and transcriptome integration points to smooth muscle cell involvement in women.

Sex differences are evident in the clinical presentation and underlying histology of atherosclerotic disease with women developing more stable atherosclerotic lesions than men. It is unknown whether this is explained by sex differences in gene regulation in cellular compartments of atherosclerotic plaques. To study sex differences in gene regulation we performed genome-wide DNA methylation and transcriptomics analysis on plaques of 485 carotid endarterectomy patients (31% female). Sex-differential DNA methylation at 4,848 sites in the autosome was enriched for cell-fate commitment and developmental processes, and its deconvolution predicted more smooth muscle cells in females, as compared to more immune cells in males. RNA-sequencing of the same plaques corroborated the sex differences in DNA methylation predicted cell-types, in which genes that were higher expressed in females were enriched for TGF-beta signaling and extracellular matrix biology. In addition, female-biased genes were enriched for targeting by regulatory loci based on sex differential methylation. Lastly, by using single-cell RNA sequencing we showed that these female-biased genes are mostly expressed in smooth muscle cells, and higher expressed in smooth muscle cells from female (predominantly stable) plaques as compared to male (relatively unstable) plaques. Our approach identified female-biased genes in smooth muscle cells in fibrous atherosclerotic plaques. This points towards new mechanisms in smooth muscle cell biology of stable atherosclerotic plaques and offers new directions for research to develop new sex-specific therapeutics for atherosclerotic disease.

genomics↗

Exploring the Causal Effects of Shear Stress Associated DNA Methylation on Cardiovascular Risk

Background and aimsAtherosclerosis is a lipid-driven inflammatory disease presumably initiated by endothelial activation. Low vascular shear stress is known for its ability to activate endothelial cells. Differential DNA methylation (DNAm) is a relatively unexplored player in atherosclerotic disease development and endothelial dysfunction. Literature search revealed that expression of 11 genes have been found to be associated with differential DNAm due to low shear stress in endothelial cells. We hypothesized a causal relationship between DNAm of shear stress associated genes in human carotid plaque and increased risk of cardiovascular disease. MethodsUsing Mendelian randomisation (MR) analysis, we explored the potential causal role of DNAm of shear stress associated genes on cardiovascular disease risk. We used genetic and DNAm data of 442 carotid endarterectomy derived advanced plaques from the Athero-Express Biobank Study for quantitative trait loci (QTL) discovery and performed MR analysis using these QTLs and GWAS summary statistics of coronary artery disease (CAD) and ischemic stroke (IS). ResultsWe discovered 9 methylation QTLs in plaque for differentially methylated shear stress associated genes. We found no significant effect of shear stress gene promotor methylation and increased risk of CAD and IS. ConclusionsDifferential methylation of shear stress associated genes in advanced atherosclerotic plaques in unlikely to increase cardiovascular risk. Highlights- Plaque-derived DNA methylation in shear stress associated genes shows no significant effect on cardiovascular disease - Genetic variants in shear stress associated genes affect DNA methylation in human carotid plaque - Human validation of atherosclerotic associated genes in murine models

genetics↗

Polygenic Susceptibility of Aortic Aneurysms Associates to the Diameter of the Aneurysm Sac: the Aneurysm-Express Biobank Cohort.

PurposeAbdominal aortic aneurysms (AAA) have a multifactorial pathology with both genetic and environmental risk factors. Recent genome-wide association studies (GWAS) have discovered ten genetic risk loci for AAA. To what extent these genetic loci contribute to the aneurysm pathology is yet unknown. This study aims to investigate whether genetic risk variants are associated with three clinical features: diameter of aneurysm sac, type of artery and symptoms.\n\nMethodsWe used aneurysm tissue from 415 patients included within the Aneurysm-Express biobank. A best fit polygenic risk score (PRS) based on previous GWAS effect size estimates was modeled for each clinical parameter by comparing model predictions across different p-value thresholds. Next, the established 10 risk variants for AAA were tested individually for association with selected clinical phenotypes. Models were corrected for age, sex, ancestral background, smoking status and diameter of the aneurysm sac or artery type if applicable, and data was normalized.\n\nResultsThe best fit PRS (including 272 SNPs with PT=0.01015) showed a significant correlation with diameter of the aneurysm sac (R2 = 0.019, p = 0.001). No association was found with clinical symptoms or type of artery. Individual variant analysis showed no clear associations with any of the clinical features.\n\nConclusionsWithin the Aneurysm-Express Biobank Study, a weighted polygenic score of AAA susceptibility explained 1.9% of the phenotypic variation (p = 0.001) in aneurysm diameter. Individual risk variant analysis showed no clear associations. Given our limited sample size, future biobank collaborations need to confirm a potential causal role of individual SNPs on the pathology of aneurysms.

genetics↗

Common variants in OSMR contribute to carotid plaque vulnerability

Background and aimsOncostatin M (OSM) signaling is implicated in atherosclerosis, however the mechanism remains unclear. We investigated the impact of common genetic variants in OSM and its receptors, OSMR and LIFR, on overall plaque vulnerability, plaque phenotype, intraplaque OSMR and LIFR expression, coronary artery calcification burden and cardiovascular disease susceptibility. Methods and resultsWe queried Genotype-Tissue Expression data and found that rs13168867 (C allele) was associated with decreased OSMR expression and that rs10491509 (A allele) was associated with increased LIFR expression in arterial tissues. No variant was significantly associated with OSM expression. We associated these two variants with plaque characteristics from 1,443 genotyped carotid endarterectomy patients in the Athero-Express Biobank Study. After correction for multiple testing, rs13168867 was significantly associated with an increased overall plaque vulnerability ({beta}=0.118 {+/-} s.e.=0.040, p=3.00x10-3, C allele). Looking at individual plaque characteristics, rs13168867 showed strongest associations with intraplaque fat ({beta}=0.248 {+/-} s.e.=0.088, p=4.66 x 10-3, C allele) and collagen content ({beta}=-0.259 {+/-} s.e.=0.095, p=6.22 x 10-3, C allele), but these associations were not significant after correction for multiple testing. rs13168867 was not associated with intraplaque OSMR expression. Neither was intraplaque OSMR expression associated with plaque vulnerability and no known OSMR eQTLs were associated with coronary artery calcification burden, or cardiovascular disease susceptibility. No associations were found for rs10491509 in the LIFR locus. ConclusionsOur study suggests that rs1316887 in the OSMR locus is associated with increased plaque vulnerability, but not with coronary calcification or cardiovascular disease risk. It remains unclear through which precise biological mechanisms OSM signaling exerts its effects on plaque morphology. However, the OSM-OSMR/LIFR pathway is unlikely to be causally involved in lifetime cardiovascular disease susceptibility.

genetics↗