Page 92 - GTM-2-4

Global Translational Medicine

ORIGINAL RESEARCH ARTICLE
Quantitative proteomic analysis reveals

regulatory networks of extracellular matrix
receptor interaction pathways in endothelial

cells after myocardial infarction

Xuan Wu 1,2,3,4† , Jiageng Cai 1,2,3,4† , Peng Wang 1,2,3,4 , and Lingyun Zu 1,2,3,4 *
1 Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, Beijing,
China
2 State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China
3 NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Peking University,
Beijing, China
4 Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing, China

Abstract

Cardiac fibrosis, a significant pathological alteration following myocardial infarction
(MI), remains enigmatic with respect to the role of cardiac endothelial cells (ECs).
To elucidate the proteomic shifts in cardiac ECs accompanying MI-induced cardiac
fibrosis, a standard MI mice model was established through ligation of the left anterior
† These authors contributed equally descending branch. Following 14 days of effective modeling, we isolated primary ECs
to this work. from the hearts of both sham and MI models utilizing the CD31 microbeads sorting
*Corresponding author: technique. Quantitative proteomics and bioinformatics methodologies, including
Lingyun Zu tandem mass spectrometry, were employed to discern proteomic alterations in
(dr_zly@126.com) the primary endothelial cells of the experimental groups. Comprehensive analyses,

Citation: Wu X, Cai J, Wang P, including Gene Ontology analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG)
et al., 2023, Quantitative proteomic analysis, functional enrichment analysis, and functional enrichment cluster analysis,
analysis reveals regulatory
networks of extracellular matrix revealed an up-regulation of proteins associated with extracellular matrix-receptor
receptor interaction pathways in interaction pathway in cardiac fibrosis post-MI. Subsequent Western blot analysis
endothelial cells after myocardial confirmed the up-regulation of specific proteins involved in this pathway, namely
infarction. Global Transl Med, 2(4):
2217. collagen type VI alpha 2 (Col6α2), vitronectin (Vtn), and integrin beta (Itgβ). We
https://doi.org/10.36922/gtm.2217 conclude that the expression levels of Col6α2, Vtn, and Itgβ in primary ECs during the
early stage of cardiac fibrosis, 14 days post-MI, were significantly elevated compared
Received: November 9, 2023
Accepted: December 20, 2023 to the sham group (P < 0.05). This observation suggests that ECM-receptor interaction
Published Online: December 29, 2023 could potentially influence the progression of cardiac fibrosis following MI.
Copyright: © 2023 Author(s).
This is an Open-Access article
distributed under the terms of the Keywords: Myocardial infarction; Cardiac fibrosis; Endothelial cells; Proteomics;
Creative Commons Attribution Extracellular matrix receptor
License, permitting distribution,
and reproduction in any medium,
provided the original work is
properly cited.
1. Introduction
Publisher’s Note: AccScience
Publishing remains neutral with The current landscape sees coronary heart disease as a predominant clinical manifestation
regard to jurisdictional claims in
published maps and institutional of cardiovascular disease. Acute myocardial infarction (MI) poses a substantial risk
affiliations. as a secondary disease, with the potential for dire consequences, including direct

Volume 2 Issue 4 (2023) 1 https://doi.org/10.36922/gtm.2217