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.
Keyphrases
- wild type
- rheumatoid arthritis
- disease activity
- ankylosing spondylitis
- interstitial lung disease
- oxidative stress
- drug induced
- escherichia coli
- diabetic rats
- systemic lupus erythematosus
- type diabetes
- systemic sclerosis
- early onset
- binding protein
- metabolic syndrome
- south africa
- density functional theory
- electronic health record
- high fat diet induced
- idiopathic pulmonary fibrosis
- artificial intelligence
- long non coding rna
- stress induced