{
  "abstract": "Introduction Carotid stenosis is a result of buildup of plaques in the carotid arteries which could lead to stroke. Although prior histological studies have led to better characterization of atherosclerotic plaque compositions, a mechanistic pathway exploring the roles played by different cell types in plaque formation and the pathways thereof have still not been explored.Objective The aim of this study is to sample cells from the region of atherosclerotic plaque during endovascular treatment and identify differentially expressed genes (DEGs) between control and atherosclerosis cases. Furthermore, we aim to identify significant pathways of each cell type.Methods Endovascular cell biopsies of internal carotid arteries with atherosclerotic disease were obtained using angioplasty balloons and the stent deployment platforms. Cells were mechanically dissociated and isolated for 10x single cell RNA sequencing. After accounting for doublets and cells with low gene counts (<500 genes), cells were annotated using a set of marker genes for different types of cells. For each cell type, we used DESeq2 to identify differentially expressed genes (DEGs) in pseudo-bulked samples between control and AP cases. Furthermore, we performed functional profiling using gProfiler to identify significantly enriched biological processes using the DEGs.Results We analyzed a total of 8 samples (2 control and 6 atherosclerosis cases) with 112417 cells. In the current analysis, we primarily focused on monocytes and macrophages since these are cell types implicated in AP growth and progression. In our analysis of 19444 monocytes (15533 atherosclerosis and 3911 control), we observed that 54 DEGs were upregulated and 1 gene was downregulated in atherosclerosis. Pathway analysis revealed that blood coagulation, platelet activation, and chemokine responses were significantly enriched. This suggests local inflammation due to high immune activity and an activated state of the monocytes potentially leading to transmigration through the endothelium leading to atherosclerosis formation and growth. Through our analysis of 4399 macrophages (3573 atherosclerosis and 826 control) we observed 22 DEGs were upregulated. Pathway analysis showed that there was high inflammatory activity, immune cell recruitment, and plaque instability through granulocyte migration and platelet activation.Conclusion We observed that scRNAseq of atherosclerotic plaques can reveal novel pathways for early detection of carotid plaque formation.Disclosures S. Veeturi: None. S. Dabb: None. K. Budohoski: None.Abstract E-259 Figure 1A) Volcano plot differentially expressed genes in monocytes between control and atherosclerosis. B) Dot plot of enriched pathways in monocytes between control and atherosclerosis monocytes",
  "authors": [
    {
      "affiliations": [
        "Neurosurgery, University of Utah, Salt Lake City, UT"
      ],
      "name": "S Veeturi"
    },
    {
      "affiliations": [
        "Neurosurgery, University of Utah, Salt Lake City, UT"
      ],
      "name": "S Dabb"
    },
    {
      "affiliations": [
        "Neurosurgery, University of Utah, Salt Lake City, UT"
      ],
      "name": "AS Liang"
    },
    {
      "affiliations": [
        "Neurosurgery, University of Utah, Salt Lake City, UT"
      ],
      "name": "K Budohoski"
    }
  ],
  "title": "E-259 Novel pathways for plaque formation in patients with carotid stenosis: a preliminary single cell sequencing analysis",
  "uid": "432361e4-8085-58c0-ab70-dc8cc3bea510"
}