DNA Methyltransferase 3b Accelerates the Process of Atherosclerosis.


Journal

Oxidative medicine and cellular longevity
ISSN: 1942-0994
Titre abrégé: Oxid Med Cell Longev
Pays: United States
ID NLM: 101479826

Informations de publication

Date de publication:
2022
Historique:
received: 08 01 2022
accepted: 09 03 2022
entrez: 15 4 2022
pubmed: 16 4 2022
medline: 19 4 2022
Statut: epublish

Résumé

DNA methylation plays a key role in establishing cell type-specific gene expression profiles and patterns in atherosclerosis. The underlying mechanism remains unclear. Previous studies have shown that DNA methyltransferase 3b (DNMT3b) may play an important role in atherosclerosis. This study aimed to establish the regulatory role of DNMT3b in the development of atherosclerosis. We constructed a viral vector carrying Dnmt3b shRNA to transduce ApoE It showed that Dnmt3b silencing attenuated atherosclerosis, including decreased lesion size and macrophage content and increased collagen and smooth muscle cells content in ApoE DNMT3b accelerated atherosclerosis, and may be associated with FOXP3 hypermethylation status in regulatory T cells.

Sections du résumé

Background UNASSIGNED
DNA methylation plays a key role in establishing cell type-specific gene expression profiles and patterns in atherosclerosis. The underlying mechanism remains unclear. Previous studies have shown that DNA methyltransferase 3b (DNMT3b) may play an important role in atherosclerosis. This study aimed to establish the regulatory role of DNMT3b in the development of atherosclerosis.
Methods UNASSIGNED
We constructed a viral vector carrying Dnmt3b shRNA to transduce ApoE
Results UNASSIGNED
It showed that Dnmt3b silencing attenuated atherosclerosis, including decreased lesion size and macrophage content and increased collagen and smooth muscle cells content in ApoE
Conclusions UNASSIGNED
DNMT3b accelerated atherosclerosis, and may be associated with FOXP3 hypermethylation status in regulatory T cells.

Identifiants

pubmed: 35422896
doi: 10.1155/2022/5249367
pmc: PMC9005271
doi:

Substances chimiques

Apolipoproteins E 0
Forkhead Transcription Factors 0
RNA, Small Interfering 0
DNA (Cytosine-5-)-Methyltransferases EC 2.1.1.37

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

5249367

Informations de copyright

Copyright © 2022 Ling Zhu et al.

Déclaration de conflit d'intérêts

All the authors declare there is no conflict of interest.

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Auteurs

Ling Zhu (L)

Department of Cardiology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi 710000, China.
Department of Cardiology, The Third Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710000, China.

Lei Jia (L)

Department of Cardiology, State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China.

Na Liu (N)

Department of Pediatric Cardiology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi 710000, China.

Runmiao Wu (R)

Department of Respiratory and Critical Care Medicine, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi 710000, China.

Gongchang Guan (G)

Department of Cardiology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi 710000, China.

Rutai Hui (R)

Department of Cardiology, State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China.

Yujie Xing (Y)

Department of Cardiology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi 710000, China.

Yong Zhang (Y)

Department of Cardiology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi 710000, China.

Junkui Wang (J)

Department of Cardiology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi 710000, China.

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Classifications MeSH