Transcriptomic and Multi-scale Network Analyses Reveal Key Drivers of Cardiovascular Disease

Bat-Ider Tumenbayar1, Khanh Pham2, John C Biber2

  • 1Department of Pharmacology and Toxicology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, NY 14203, USA.

Insights

Vascular injury in mice alters gene expression and molecular networks, mimicking cardiovascular diseases (CVDs). This study validates the fine-wire injury model for investigating CVD mechanisms and potential treatments.

Area of Science:

  • Molecular biology
  • Bioinformatics
  • Cardiovascular research

Background:

  • Cardiovascular diseases (CVDs) involve molecular signaling, extracellular matrix (ECM), cytoskeleton, and immune responses.
  • The fine-wire vascular injury model is used for neointimal hyperplasia but not typically for CVDs.

Purpose of the Study:

  • To test the hypothesis that vascular injury induces CVD-like changes at transcriptome and protein levels.
  • To analyze gene expression and molecular communication in a mouse vascular injury model.

Main Methods:

  • Microarray analysis of injured vs. uninjured mouse femoral arteries.
  • Construction of protein-protein interaction networks and identification of functional clusters.
  • Machine learning-based disease pathway analysis.

Main Results:

  • Identified 1,467 differentially expressed genes linked to CVDs like atherosclerosis and vaso-occlusion.
  • Discovered seven distinct protein interaction clusters enriched in ECM, metabolism, cytoskeleton, and immune response.
  • Revealed crosstalk between ECM remodeling, immune response, and cytoskeleton reorganization linked to various CVD pathologies.

Conclusions:

  • Vascular injury model effectively replicates transcriptomic and molecular network changes seen in CVDs.
  • The model's robustness supports its use for studying cardiovascular disease mechanisms.
  • Highlights the interconnected roles of ECM, cytoskeleton, and immune response in vascular pathologies.