SNRNP70 is Associated with Focal Adhesion-Related Signatures and Chondrocyte Inflammation in Osteoarthritis

Osteoarthritis (OA) is a degenerative joint disease marked by progressive cartilage breakdown and synovial inflammation, yet the key molecular drivers of its pathogenesis remain incompletely understood. Here, the examination was conducted as to whether SNRNP70-a core component of the U1 snRNP complex essential for pre‑mRNA splicing-contributes to OA progression. Analysis of ten public transcriptomic datasets showed that SNRNP70 was consistently downregulated in OA cartilage compared with normal controls. A meta‑analysis further indicated good diagnostic accuracy for OA, with a pooled AUC of 0.92. In primary rat chondrocytes stimulated with interleukin‑1β (IL‑1β), SNRNP70 expression was suppressed under inflammatory conditions. Forced expression of SNRNP70 not only reduced the production of pro‑inflammatory mediators (IL‑6 and MMP‑13) but also restored key extracellular matrix (ECM) components (ACAN and COL2A1) and promoted chondrocyte migration and wound healing. Pearson's correlation, followed by KEGG enrichment, indicated that focal adhesion signaling was a pathway associated with SNRNP70 regulation. Rescue experiments supported the notion that SNRNP70 enhances chondrocyte reparative capacity, at least in part, by activating this pathway. Together, these findings suggest that SNRNP70 may serve as a previously unrecognized regulator of inflammatory chondrocyte function and cartilage homeostasis. They also raise the possibility of a mechanistic link between spliceosome activity and focal adhesion‑mediated matrix synthesis, warranting further evaluation of SNRNP70 as a candidate diagnostic marker or therapeutic target in OA.