{
  "abstract": "Introduction Integrins maintain a functional vascular system by mediating ECM adhesion via interactions with ligands. 1 Integrin dysfunction can disrupt cell adhesion and influence vascular remodelling in diseases such as atherosclerosis,1 so understanding the underlying signalling mechanisms is important for the development of novel therapies. Vascular smooth muscle cells express several β1 integrins which are implicated in the phenotypic switching from a contractile cell type to foam cell and development of a fibrous plaque characteristic of atherosclerosis.2 We hypothesise integrin mechanosensing can be modulated through receptor binding to arterial wall proteoglycans, hence modulating phenotype and disease progression.Methods We present a biomimetic platform using versatile DNA origami to produce surfaces with nanoscale resolution and control over ligand spacing at single molecule level to investigate the role of integrin-receptor crosstalk in mechanosensation and arterial disease. DNA origami was functionalised with Arg-Gly-Asp Acid (RGD) peptides, a β1 aptamer or the proteoglycan chondroitin sulfate.Results When vSMCs were plated onto ligand-decorated DNA origami, confocal microscopy analysis determined that an inter-ligand spacing of ~40 nm caused an increase in cell spreading and adhesion formation. Simultaneous engagement of the β1 aptamer with chondroitin sulfate enabled the examination of adhesion formation, phosphotyrosine expression, and cell spreading due to integrin-receptor crosstalk.Conclusion We highlight the importance of precise nanoscale arrangement of integrins and ligands required for the integrin-dependent biological activities of vSMCs, providing novel insights into their integrin adhesions during atherosclerosis. Our platform has great potential in cardiovascular research and in the development of novel therapeutics - providing a highly customisable method for examining integrin-ligand interactions at the molecular level.References Lawkowska K, Bonowicz K, et al. Biomolecules. 2025;6:233A. Finney C, Stokes KY, et al. Cell Mol Life Sci. 2017;74:2263–2282.",
  "authors": [
    {
      "affiliations": [
        "School of Engineering and Materials Science, Queen Mary University of London"
      ],
      "name": "Rachel Smyth"
    },
    {
      "affiliations": [
        "School of Physical and Chemical Sciences, Queen Mary University of London"
      ],
      "name": "Matteo Palma"
    },
    {
      "affiliations": [
        "School of Engineering and Materials Science, Queen Mary University of London"
      ],
      "name": "Thomas Iskratsch"
    }
  ],
  "title": "P7  Development of a biochip for dissection of multivalent atherosclerosis signalling",
  "uid": "c638a5d1-63b7-5ae0-a598-0ce10281e1b2"
}