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Early Injury Landscape in Vein Harvest by Single-Cell and Spatial Transcriptomics.

Marina E Michaud1, Lucas Mota2, Mojtaba Bakhtiari1

  • 1Department of Pediatrics, Emory School of Medicine, Atlanta, GA (M.E.M., M.B., B.E.T., S.S.B., M.K.B.).

Circulation Research
|May 29, 2024
PubMed
Summary
This summary is machine-generated.

Vein graft harvest and implantation trigger genomic responses and maladaptive pathways, contributing to bypass graft failure. Identifying these early molecular changes offers potential therapeutic targets for improving graft survival.

Keywords:
coronary artery bypassendotheliumhyperplasiasingle-cell analysisspatial analysisvascular grafting

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Area of Science:

  • Vascular Biology
  • Genomics
  • Surgical Pathology

Background:

  • Vein graft failure after cardiovascular bypass surgery causes significant morbidity and healthcare costs.
  • Injury during vein graft harvest, preparation, and implantation leads to intimal hyperplasia, stenosis, and eventual failure.
  • Specific signaling pathways during vein graft preparation remain undefined, potentially cumulatively impacting graft outcomes.

Purpose of the Study:

  • To elucidate the genomic response of the vein conduit wall during harvest and implantation.
  • To identify key maladaptive pathways driving vein graft failure.
  • To discover potential therapeutic targets for biologic intervention against surgical vein graft injury.

Main Methods:

  • Utilized single-nuclei RNA-sequencing and spatial transcriptomics.
  • Profiled genomic effects in canine vein grafts after harvest, distension, and 24-hour post-implantation bypass.
  • Analyzed cellular subpopulations, gene expression, and intercellular communication networks.

Main Results:

  • Spatial transcriptomics revealed activated ECs, fibroblasts, and VSMCs, with enriched proliferation, migration, and ECM remodeling pathways.
  • Single-nuclei RNA-sequencing identified distinct EC and fibroblast subpopulations with upregulated injury response and activation markers.
  • Post-implantation grafts showed increased myeloid and protomyofibroblast cells, with upregulated genes like VCAN, FBN1, VEGFC, GLIS3, and EPHA3, driving pathological pathways (e.g., IL-6, TGFBR1).

Conclusions:

  • Vein graft harvest and distension initiate a prompt genomic response involving diverse cellular subpopulations.
  • This response is exacerbated post-implantation, activating maladaptive gene regulatory networks contributing to graft failure.
  • Distension upregulates pathological pathways, presenting potential early therapeutic targets for vein graft failure.