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Published in: Cardiovascular Toxicology 9-10/2023

16-08-2023 | Atrial Fibrillation

COMP Improves Ang-II-Induced Atrial Fibrillation via TGF-β Signaling Pathway

Authors: XiaoBi Cai, Mingliang Li, Ying Zhong, Wenkun Yang, Zhu Liang

Published in: Cardiovascular Toxicology | Issue 9-10/2023

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Abstract

Cartilage oligomeric matrix protein (COMP) regulates transforming growth factor-β (TGF-β) signaling pathway, which has been proved to be associated with skin fibrosis and pulmonary fibrosis. Atrial fibrosis is a major factor of atrial fibrillation (AF). Nevertheless, the interaction between COMP and TGF-β as well as their role in AF remains undefined. The purpose of this study is to clarify the role of COMP in AF and explore its potential mechanism. The hub gene of AF was identified from two datasets using bioinformatics. Furthermore, it was verified by the downregulation of COMP in angiotensin-II (Ang-II)-induced AF in mice. Moreover, the effect on AF was examined using CCK8 assay, ELISA, and western blot. The involvement of TGF-β pathway was further discussed. The expression of COMP was the most significant among all these hub genes. Our experimental results revealed that the protein levels of TGF-β1, phosphorylated Smad2 (P-Smad2), and phosphorylated Smad3 (P-Smad3) were decreased after silencing COMP, which indicated that COMP knockdown could inhibit the activation of TGF-β pathway in AF cells. However, the phenomenon was reversed when the activator SRI was added. COMP acts as a major factor and can improve Ang-II-induced AF via TGF-β signaling pathway. Thus, our research enriches the understanding of the interaction between COMP and TGF-β in AF, and provides reference for the pathogenesis and diagnosis of AF.
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Metadata
Title
COMP Improves Ang-II-Induced Atrial Fibrillation via TGF-β Signaling Pathway
Authors
XiaoBi Cai
Mingliang Li
Ying Zhong
Wenkun Yang
Zhu Liang
Publication date
16-08-2023
Publisher
Springer US
Published in
Cardiovascular Toxicology / Issue 9-10/2023
Print ISSN: 1530-7905
Electronic ISSN: 1559-0259
DOI
https://doi.org/10.1007/s12012-023-09799-1

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