Epigenetics in rheumatoid arthritis; fibroblast-like synoviocytes as an emerging paradigm in the pathogenesis of the disease.


Journal

Immunology and cell biology
ISSN: 1440-1711
Titre abrégé: Immunol Cell Biol
Pays: United States
ID NLM: 8706300

Informations de publication

Date de publication:
03 2020
Historique:
received: 15 05 2019
revised: 14 12 2019
accepted: 16 12 2019
pubmed: 20 12 2019
medline: 18 11 2020
entrez: 20 12 2019
Statut: ppublish

Résumé

Rheumatoid arthritis (RA) is characterized by immune dysfunctions and chronic inflammation that mainly affects diarthrodial joints. Genetics has long been surveyed in searching for the etiopathogenesis of the disease and partially clarified the conundrums within this context. Epigenetic alterations, such as DNA methylation, histone modifications, and noncoding RNAs, which have been considered to be involved in RA pathogenesis, likely explain the nongenetic risk factors. Epigenetic modifications may influence RA through fibroblast-like synoviocytes (FLSs). It has been shown that FLSs play an essential role in the onset and exacerbation of RA, and therefore, they may illustrate some aspects of RA pathogenesis. These cells exhibit a unique DNA methylation profile in the early stage of the disease that changes with disease progression. Histone acetylation profile in RA FLSs is disrupted through the imbalance of histone acetyltransferases and histone deacetylase activity. Furthermore, dysregulation of microRNAs (miRNAs) is immense. Most of these miRNAs have shown an aberrant expression in FLSs that are involved in proliferation and cytokine production. Besides, dysregulation of long noncoding RNAs in FLSs has been revealed and attributed to RA pathogenesis. Further investigations are needed to get a better view of epigenetic alterations and their interactions. We also discuss the role of these epigenetic alterations in RA pathogenesis and their therapeutic potential.

Identifiants

pubmed: 31856314
doi: 10.1111/imcb.12311
doi:

Substances chimiques

Histones 0
MicroRNAs 0
RNA, Long Noncoding 0
Histone Acetyltransferases EC 2.3.1.48
Histone Deacetylases EC 3.5.1.98

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

171-186

Informations de copyright

© 2019 Australian and New Zealand Society for Immunology Inc.

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Auteurs

Jafar Karami (J)

Rheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Department of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Department of Laboratory Sciences, Khomein University of Medical Sciences, Khomein, Iran.

Saeed Aslani (S)

Rheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.

Mohammad Naghi Tahmasebi (MN)

Department of Orthopedics, Division of Knee Surgery, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran.

Mohammad Javad Mousavi (MJ)

Department of Hematology, Faculty of Allied Medicine, Bushehr University of Medical Sciences, Bushehr, Iran.
Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

Arash Sharafat Vaziri (A)

Department of Orthopedics, Division of Knee Surgery, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran.

Ahmadreza Jamshidi (A)

Rheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.

Elham Farhadi (E)

Rheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Inflammation Research Center, Tehran University of Medical Sciences, Tehran, Iran.

Mahdi Mahmoudi (M)

Rheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Inflammation Research Center, Tehran University of Medical Sciences, Tehran, Iran.

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