FUS regulates the alternative splicing of cell proliferation genes related to atherosclerosis.


Journal

Experimental biology and medicine (Maywood, N.J.)
ISSN: 1535-3699
Titre abrégé: Exp Biol Med (Maywood)
Pays: England
ID NLM: 100973463

Informations de publication

Date de publication:
Sep 2023
Historique:
pmc-release: 09 03 2024
medline: 27 11 2023
pubmed: 9 9 2023
entrez: 9 9 2023
Statut: ppublish

Résumé

FUS plays a significant role as an RNA-binding protein in several cellular processes, including RNA splicing, DNA repair, and transcriptional regulation. However, the RNA-binding capacity of FUS in atherosclerosis is unclear. We aimed to study the functions of FUS in inflammatory regulation through the role of the splicing factor. We knocked down FUS with siRNA to further study the overall transcriptional level and select alternative splicing (AS) of FUS regulation in human umbilical vein endothelial cells (HUVECs) by RNA sequencing. The results suggested that the knockdown of FUS significantly affected gene expression in HUVECs. In addition, the knockdown of FUS resulted in 200 differentially expressed genes (DEGs) that were highly related to apoptotic process, signal transduction, multicellular organism development, cell adhesion and regulation of transcription, and DNA-templated pathways. Importantly, FUS extensively regulated 2870 AS events with a significant difference. Functional analysis of its modulated AS genes revealed they were highly enriched in cell cycle and cell population proliferation pathways. The qRT-PCR and RNA-seq data showed consistent results. Our findings suggested new knowledge of the mechanisms of FUS associated with atherosclerosis.

Identifiants

pubmed: 37688506
doi: 10.1177/15353702231187642
pmc: PMC10666725
doi:

Substances chimiques

RNA, Small Interfering 0
FUS protein, human 0
RNA-Binding Protein FUS 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1459-1468

Déclaration de conflit d'intérêts

Declaration of Conflicting InterestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

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Auteurs

Jianjun Hou (J)

Department of Cardiology, General Hospital of Ningxia Medical University, Yinchuan 750000, China.

Shaobing Yang (S)

Department of Cardiology, General Hospital of Ningxia Medical University, Yinchuan 750000, China.

Ying Guo (Y)

Department of Cardiology, General Hospital of Ningxia Medical University, Yinchuan 750000, China.

Ning Yan (N)

Department of Cardiology, General Hospital of Ningxia Medical University, Yinchuan 750000, China.

Shaobin Jia (S)

Department of Cardiology, General Hospital of Ningxia Medical University, Yinchuan 750000, China.

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Classifications MeSH