FTO-mediated RNA m6A methylation regulates synovial aggression and inflammation in rheumatoid arthritis

Biochim Biophys Acta Mol Basis Dis. 2024 Oct;1870(7):167341. doi: 10.1016/j.bbadis.2024.167341. Epub 2024 Jul 16.

Abstract

Fibroblast-like synoviocytes (FLS) plays an important role in synovial inflammation and joint damage in rheumatoid arthritis (RA). As the most abundant mRNA modification, N6-methyladenosine (m6A) is involved in the development of various diseases; however, its role in RA remains to be defined. In this study, we reported the elevated expression of the m6A demethylase fat mass and obesity-associated protein (FTO) in FLS and synovium from RA patients. Functionally, FTO knockdown or treatment with FB23-2, an inhibitor of the mRNA m6A demethylase FTO, inhibited the migration, invasion and inflammatory response of RA FLS, however, FTO-overexpressed RA FLS exhibited increased migration, invasion and inflammatory response. We further demonstrated that FTO promoted ADAMTS15 mRNA stability in an m6A-IGF2BP1 dependent manner. Notably, the severity of arthritis was significantly reduced in CIA mice with FB23-2 administration or CIA rats with intra-articular injection of FTO shRNA. Our results illustrate the contribution of FTO-mediated m6A modification to joint damage and inflammation in RA and suggest that FTO might be a potential therapeutic target in RA.

Keywords: ADAMTS15; FTO; Fibroblast-like synoviocytes; Invasion; Migration; Rheumatoid arthritis; m(6)A modification.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine* / analogs & derivatives
  • Adenosine* / metabolism
  • Alpha-Ketoglutarate-Dependent Dioxygenase FTO* / genetics
  • Alpha-Ketoglutarate-Dependent Dioxygenase FTO* / metabolism
  • Animals
  • Arthritis, Experimental / genetics
  • Arthritis, Experimental / metabolism
  • Arthritis, Experimental / pathology
  • Arthritis, Rheumatoid* / genetics
  • Arthritis, Rheumatoid* / metabolism
  • Arthritis, Rheumatoid* / pathology
  • Humans
  • Inflammation* / genetics
  • Inflammation* / metabolism
  • Inflammation* / pathology
  • Mice
  • RNA Methylation*
  • RNA Stability
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Rats
  • Synovial Membrane / metabolism
  • Synovial Membrane / pathology
  • Synoviocytes / metabolism
  • Synoviocytes / pathology

Substances

  • Adenosine
  • Alpha-Ketoglutarate-Dependent Dioxygenase FTO
  • FTO protein, human
  • N-methyladenosine
  • RNA, Messenger