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Lack of Syndecan-1 promotes the pathogenesis of experimental rheumatoid arthritis

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Abstract

Syndecan-1 (Sdc-1), a transmembrane heparan sulfate protein, is implicated in several pathophysiological processes including rheumatoid arthritis (RA). The exact role of Syndican-1 in this autoimmune disease is still undetermined. This study explores the involvement level of Sdc-1 in the development of RA in a collagen II–induced arthritis mice model. RA was induced in two mice strains (wild-type BALB/c group and Sdc-1 knockout) by collagen II. Mice underwent regular clinical observations and scoring. After sacrifice, leg biopsies were taken from mice for histological examination, using a variety of stains. In addition, proteins were extracted, and molecular assessment of TNF-α was performed using the western blot technique. In the Sdc-1 knockout group, clinical scoring results showed a significantly more severe experimental RA; histology showed a significant increase in bone erosion, cartilage destruction, inflammation, and less granulated mast cells than the wild-type. In addition, molecular assessment of TNF-α showed more increase in expression in the Sdc-1 knockout models compared to the wild-type. Data suggest that lack of Sdc-1 enhances the inflammatory characteristics in RA. However, more molecular studies and investigations are needed to determine its exact role and possible mechanisms involved.

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Acknowledgements

The Syndecan-1 knockout mice were gifted from Professor Marie Anne Stepp, from the Department of Anatomy and Cell Biology, George Washington University, Washington DC, USA.

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Grant from the Medical Practice Plan of the American University of Beirut Medical Center in 2019 (MPP-2019/20).

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Correspondence to Abdo Jurjus.

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The study was approved by the Institutional Animal Care and Use Committee of the American University of Beirut, Lebanon (IACUC# 19-09-552).

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The authors declare no competing interests.

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Jurjus, R., Dosh, L., Farhat, R. et al. Lack of Syndecan-1 promotes the pathogenesis of experimental rheumatoid arthritis. Immunogenetics (2024). https://doi.org/10.1007/s00251-024-01337-9

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  • DOI: https://doi.org/10.1007/s00251-024-01337-9

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