Article Text

Download PDFPDF

72 Implications of autophagy for functinal changes of rheumatoid arthritis fibroblast-like synoviocytes
  1. JM Kim1,
  2. J Bang2,
  3. YG Jeong3,
  4. CH Lee4,
  5. CN Son1 and
  6. SH Kim1
  1. 1Keimyung University Dongsan Medical Centre, Division of Rheumatology- Department of Internal Medicine, Daegu, Republic of Korea
  2. 2Keimyung University Graduate School, Medicine, Daegu, Republic of Korea
  3. 3Changwon Fatima Hospital, Division of Rheumatology- Department of Internal Medicine, Changwon, Republic of Korea
  4. 4School of Medicine- Wonkwang University, Division of Rheumatology- Department of Internal Medicine, Iksan, Republic of Korea


Background and aims Rheumatoid arthritis (RA) is characterised by exaggerated synovial proliferation in which interleukin-17A (IL-17A) plays a key role. Recently several evidences support the implication of autophagy in the pathogenesis of RA. The aims of this study are (1) to evaluate whether IL-17A influences on autophagic flux in RA synovium and (2) to investigate whether the modulation of autophagy can regulate migration and proliferation of fibroblast-like synoviocytes (FLS) from the patients with RA (RA-FLS) under inflammatory milieu.

Methods FLS from the patients with RA or osteoarthritis (OA) were cultured with IL-17A and/or autophagy regulators. The expression of marker proteins for autophagic flux or the formation of autophagolysosome was analysed by western blot or immunofluorescence study. A migration scratch assay was used to assess FLS migration. Proliferation of FLS was determined by the viable cell count using trypan blue.

Results LC3 conversion from LC3-I to LC3-II was increased in RA-FLS than in OA-FLS. IL-17A upregulated the expression of LC3B, Atg5, Beclin1, LAMP1 in RA-FLS. The accumulation of p62 was also prominent in RA-FLS. Migration and proliferation of FLS stimulated by IL-17A was suppressed by Bafilomycin A1 which prevented the formation of autophagolysosomes. P62-silencing enhanced IL-17A-induced autophagy activation in RA-FLS.

Conclusions This study reveals that IL-17A stimulates autophagy and that intervention of autophagy can control IL-17A-induced migration and proliferation of FLS. Our results also provide additional evidence for a significant role of autophagy in the pathogenesis of RA. Thus, we suggest that autophagy might be a potential therapeutic target for the management of RA.

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.