Publications by authors named "Noortje A M van den Dungen"

N6-methyladenosine (m6A) is a RNA modification that can regulate post-transcriptional processes including RNA stability, translation, splicing, and nuclear export. In CD4+ lymphocytes, m6A modifications have been demonstrated to play a role in early differentiation processes. The role of m6A in CD4+ T cell activation and effector function remains incompletely understood.

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  • Histopathological studies of atherosclerotic plaques reveal that diverse lesion types necessitate improved classification methods to understand their clinical significance.
  • An analysis of gene expression in 654 human carotid plaques identified five main plaque types, each linked to specific clinical outcomes and differences in cell composition.
  • Findings suggest that a particular plaque type with severe symptoms is associated with inflammatory and fibrotic cells, and ongoing research is exploring potential biomarkers for distinguishing these plaque phenotypes.
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  • Myofibroblasts in atherosclerotic plaques play a vital role in disease progression by producing extracellular matrix and contributing to the structure of plaques, yet smooth muscle cells are often used for research instead.
  • The study introduces a new method to isolate and culture plaque myofibroblasts from 27 donors, which maintain their growth and retain characteristics of their original cellular environment.
  • This research confirms that cultured myofibroblasts closely resemble those found in plaques and can be used effectively in studies examining various mechanisms of atherosclerosis.
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  • The study investigates the role of erythrocyte membranes, specifically through the marker glycophorin C, in atherosclerotic plaques and how they may relate to plaque vulnerability and intraplaque hemorrhage (IPH).
  • Researchers analyzed samples from a large cohort of patients who underwent carotid endarterectomy, assessing various plaque features and the prevalence of IPH and neurological symptoms.
  • It was found that higher glycophorin C levels were associated with IPH and pre-procedural neurological symptoms, particularly in men, suggesting that these markers could help predict plaque instability.
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  • Vascular diseases are influenced by their specific locations in the body, highlighting the need for more research into the genetic differences that cause this variability.
  • The study analyzed cell samples from nine large blood vessels in dogs, revealing that unique gene expression patterns remain consistent even when the cells are cultured outside their body environment.
  • Results showed that differences between arterial and venous cells affect their structure, suggesting that using cells from just one type of vessel for research may not give a complete picture of vascular biology.
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T cell activation is a highly regulated process, modulated via the expression of various immune regulatory proteins including cytokines, surface receptors and co-stimulatory proteins. N-methyladenosine (mA) is an RNA modification that can directly regulate RNA expression levels and it is associated with various biological processes. However, the function of mA in T cell activation remains incompletely understood.

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Cushing's syndrome (CS) is a serious endocrine disorder that is relatively common in dogs, but rare in humans. In ~15%-20% of cases, CS is caused by a cortisol-secreting adrenocortical tumour (csACT). To identify differentially expressed genes that can improve prognostic predictions after surgery and represent novel treatment targets, we performed RNA sequencing on csACTs (n = 48) and normal adrenal cortices (NACs; n = 10) of dogs.

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Aims: Genome-wide association studies (GWASs) have discovered hundreds of common genetic variants for atherosclerotic disease and cardiovascular risk factors. The translation of susceptibility loci into biological mechanisms and targets for drug discovery remains challenging. Intersecting genetic and gene expression data has led to the identification of candidate genes.

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Chromatin immunoprecipitation and sequencing (ChIP-seq) is a well-established method to study the epigenetic profile at the genome-wide scale, including histone modifications and DNA-protein interactions. It provides valuable insights to better understand disease mechanisms. Here we present an optimized ChIP-seq protocol suitable for human cardiac tissues, especially the frozen biobanked small biopsy samples.

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Vasculature performs a critical function in tissue homeostasis, supply of oxygen and nutrients, and the removal of metabolic waste products. Vascular problems are implicated in a large variety of pathologies and accurate models resembling native vasculature are of great importance. Unfortunately, existing models do not sufficiently reflect their counterpart.

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Genome-wide association studies (GWASs) have identified many genetic risk factors for CKD. However, linking common variants to genes that are causal for CKD etiology remains challenging. By adapting self-transcribing active regulatory region sequencing, we evaluated the effect of genetic variation on DNA regulatory elements (DREs).

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Background: Genome-wide association studies (GWAS) have revealed many susceptibility loci for complex genetic diseases. For most loci, the causal genes have not been identified. Currently, the identification of candidate genes is predominantly based on genes that localize close to or within identified loci.

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