Journal
INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 90, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.intimp.2020.107182
Keywords
Rheumatoid arthritis; Long-non-coding RNAs; SNHG1; Fibroblast-like synoviocytes; PTBP1
Categories
Funding
- National Natural Science Foundation of China [81871270]
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The up-regulation of SNHG1 in RA-FLSs contributes to sustaining cell functions such as proliferation, migration, and invasion, with the interaction between SNHG1 and PTBP1 impacting the biological behavior regulation of RA-FLSs.
Fibroblast-like synoviocytes (FLSs) in rheumatoid arthritis (RA) present proliferative and aggressive cell phenotype. RA-FLSs are the essential effector cells that lead to symptoms like synovial inflammation and joint destruction. Currently, the cause of RA-FLSs involving in the pathological process of RA remains unknown. Accumulate researches have demonstrated that lncRNAs may play a critical role in regulating the biological behaviors of RA-FLSs, but the mechanism is still unclear. Here, we found that lncRNA small nucleolar RNA host gene 1 (SNHG1) is up-regulated in RA-FLSs compared with FLSs from trauma arthritis and osteoarthritis patients. The results suggest that SNHG1 in RA-FLSs helps to sustain the cellular functions of proliferation, migration and invasion. Furthermore, the regulation mechanism depends on the interaction between SNHG1 and polypyridine tract-binding protein 1 (PTBP1). This interaction influences PTBP1 expression that participates in the regulation of RA-FLSs biological behaviors. Our results suggest that up-regulated SNHG1 of RA-FLSs may contribute to synovial aggression and disease progression in RA and be favourable for RA treatment target RA-FLSs.
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