CircRNA-3302 promotes endothelial-to-mesenchymal transition via sponging miR-135b-5p to enhance KIT expression in Kawasaki disease.
Journal
Cell death discovery
ISSN: 2058-7716
Titre abrégé: Cell Death Discov
Pays: United States
ID NLM: 101665035
Informations de publication
Date de publication:
29 Jun 2022
29 Jun 2022
Historique:
received:
04
04
2022
accepted:
16
06
2022
revised:
15
06
2022
entrez:
29
6
2022
pubmed:
30
6
2022
medline:
30
6
2022
Statut:
epublish
Résumé
Endothelial-to-mesenchymal transition (EndMT) is implicated in myofibroblast-like cell-mediated damage to coronary artery wall of Kawasaki disease (KD) patients, which subsequently increases the risk of coronary artery aneurysm. Many circular RNAs (circRNAs) have been reported to be associated with cardiovascular diseases. However, the roles and underlying molecular mechanism of circRNAs in KD-associated EndMT remains indefinite. In this research, we screened out circRNA-3302 from human umbilical vein endothelial cells (HUVECs) treated by sera from healthy controls (HCs) or KD patients via circRNA sequencing (circRNA-seq). In addition, circRNA-3302 upregulation was verified in endothelial cells stimulated by KD serum and pathological KD mice modeled with Candida albicans cell wall extracts (CAWS). Moreover, in vitro experiments demonstrated that overexpression of circRNA-3302 could markedly induce EndMT, and silencing of circRNA-3302 significantly alleviated KD serum-mediated EndMT. To further explore the molecular mechanisms of circRNA-3302 inducing EndMT, RNA sequencing (RNA-seq), a dual-luciferase reporter system, nuclear and extra-nuclear RNA isolation, RT-qPCR and Western blot analyses and so on, were utilized. Our data demonstrated that circRNA-3302 contributed to the KD-associated EndMT via sponging miR-135b-5p to enhance KIT expression. Collectively, our results imply that circRNA-3302 plays an important role in KD-associated EndMT, providing new insights into minimizing the risks of developing coronary artery aneurysms.
Identifiants
pubmed: 35768408
doi: 10.1038/s41420-022-01092-4
pii: 10.1038/s41420-022-01092-4
pmc: PMC9243129
doi:
Types de publication
Journal Article
Langues
eng
Pagination
299Subventions
Organisme : National Natural Science Foundation of China (National Science Foundation of China)
ID : No. 81970435
Organisme : National Natural Science Foundation of China (National Science Foundation of China)
ID : No. 82000469
Organisme : National Natural Science Foundation of China (National Science Foundation of China)
ID : No. 82100523
Organisme : Natural Science Foundation of Zhejiang Province (Zhejiang Provincial Natural Science Foundation)
ID : LY19H030004
Informations de copyright
© 2022. The Author(s).
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