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miR-6760-5p suppresses neoangiogenesis by targeting Yes-associated protein 1 in patients with moyamoya disease undergoing indirect revascularization.

Authors :
Wen Y
Chen J
Long T
Chen F
Wang Z
Chen S
Zhang G
Li M
Zhang S
Kang H
Feng W
Wang G
Source :
Gene [Gene] 2025 Feb 10; Vol. 937, pp. 149152. Date of Electronic Publication: 2024 Dec 09.
Publication Year :
2025

Abstract

Objective: The aim of this research was to investigate the specific regulatory role of miR-6760-5p in angiogenesis in moyamoya disease.<br />Methods: HUVECs were transfected with miR-6760-5p inhibitor and mimics fragments, then subjected to assays for cell proliferation, migration, and tube formation. Subsequently, downstream target genes of miR-6760-5p were predicted and the protein expression levels of these genes were evaluated. The presence of miR-6760-5p and YAP1 was verified by a dual luciferase reporter gene test, followed by an assessment of the effects of YAP1 and miR-6760-5p on the HUVECs.<br />Results: Comparatively to the control group, increased expression of miR-6760-5p decreased cell growth, movement, and tube formation. YAP1 gene was discovered as a target controlled by miR-6760-5p, with subsequent investigation confirming YAP1 as a gene regulated by miR-6760-5p. Additionally, miR-6760-5p was found to counteract the angiogenesis-promoting effect of YAP1.<br />Conclusion: The results of this research suggest a possible link between the miR-6760-5p gene found in the cerebrospinal fluid of individuals with moyamoya disease and the process of vascularization in this particular condition. The findings indicate that miR-6760-5p may be a new molecular indicator and potential target for the diagnosis of moyamoya disease.<br />Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.<br /> (Copyright © 2024 Elsevier B.V. All rights reserved.)

Details

Language :
English
ISSN :
1879-0038
Volume :
937
Database :
MEDLINE
Journal :
Gene
Publication Type :
Academic Journal
Accession number :
39662645
Full Text :
https://doi.org/10.1016/j.gene.2024.149152