AccScience Publishing / GTM / Volume 2 / Issue 4 / DOI: 10.36922/gtm.2217

Quantitative proteomic analysis reveals regulatory networks of extracellular matrix receptor interaction pathways in endothelial cells after myocardial infarction

Xuan Wu1,2,3,4† Jiageng Cai1,2,3,4† Peng Wang1,2,3,4 Lingyun Zu1,2,3,4*
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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
Global Translational Medicine 2023, 2(4), 2217
Submitted: 9 November 2023 | Accepted: 20 December 2023 | Published: 29 December 2023
© 2023 by the Author(s). This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution 4.0 International License ( )

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 descending branch. Following 14 days of effective modeling, we isolated primary ECs from the hearts of both sham and MI models utilizing the CD31 microbeads sorting technique. Quantitative proteomics and bioinformatics methodologies, including tandem mass spectrometry, were employed to discern proteomic alterations in the primary endothelial cells of the experimental groups. Comprehensive analyses, including Gene Ontology analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, functional enrichment analysis, and functional enrichment cluster analysis, revealed an up-regulation of proteins associated with extracellular matrix-receptor interaction pathway in cardiac fibrosis post-MI. Subsequent Western blot analysis confirmed the up-regulation of specific proteins involved in this pathway, namely collagen type VI alpha 2 (Col6α2), vitronectin (Vtn), and integrin beta (Itgβ). We 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 to the sham group (P < 0.05). This observation suggests that ECM-receptor interaction could potentially influence the progression of cardiac fibrosis following MI.

Myocardial infarction
Cardiac fibrosis
Endothelial cells
Extracellular matrix receptor
National Key Research and Development Program of China
second Tibetan Plateau Scientific Expedition and Research Program (STEP)
Clinical Cohort Construction Program of Peking University Third Hospital
Key Clinical Projects of Peking University Third Hospital
Conflict of interest
The authors declare they have no competing interests.
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Global Translational Medicine, Electronic ISSN: 2811-0021 Published by AccScience Publishing