Department of Anatomy, Cell Biology and Physiological Sciences, Faculty of Medicine, American University of Beirut, Bliss Street, Beirut, 1107-2020, Lebanon.
Department of Biomedicine, Neuroscience and Advanced Diagnostic, University of Palermo, Palermo, 90127, Italy.
Immunogenetics. 2024 Jun;76(3):145-154. doi: 10.1007/s00251-024-01337-9. Epub 2024 Mar 7.
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.
Syndecan-1（Sdc-1）是一种跨膜硫酸乙酰肝素蛋白，与多种病理生理过程有关，包括类风湿关节炎（RA）。Syndican-1 在这种自身免疫性疾病中的确切作用仍未确定。本研究通过 II 型胶原诱导关节炎小鼠模型探讨 Sdc-1 在 RA 发病机制中的参与程度。通过 II 型胶原诱导两种小鼠品系（野生型 BALB/c 组和 Sdc-1 敲除组）发生 RA。对小鼠进行定期临床观察和评分。处死小鼠后，从其腿部取活检进行组织学检查，使用多种染色方法。此外，还提取了蛋白质，并使用 Western blot 技术对 TNF-α 进行了分子评估。在 Sdc-1 敲除组中，临床评分结果显示实验性 RA 明显更严重；组织学显示骨侵蚀、软骨破坏、炎症明显增加，颗粒状肥大细胞减少，与野生型相比。此外，与野生型相比，Sdc-1 敲除模型中 TNF-α 的表达增加更多。数据表明，缺乏 Sdc-1 增强了 RA 的炎症特征。然而，需要进行更多的分子研究和调查，以确定其确切作用和可能涉及的机制。
