RNA binding proteins in osteoarthritis

Abstract

Osteoarthritis (OA) is a common chronic degenerative joint disease worldwide. The pathological features of OA are the erosion of articular cartilage, subchondral bone sclerosis, synovitis, and metabolic disorder. Its progression is characterized by aberrant expression of genes involved in inflammation, proliferation, and metabolism of chondrocytes. Effective therapeutic strategies are limited, as mechanisms underlying OA pathophysiology remain unclear. Significant research efforts are ongoing to elucidate the complex molecular mechanisms underlying OA focused on gene transcription. However, posttranscriptional alterations also play significant function in inflammation and metabolic changes related diseases. RNA binding proteins (RBPs) have been recognized as important regulators in posttranscriptional regulation. RBPs regulate RNA subcellular localization, stability, and translational efficiency by binding to their target mRNAs, thereby controlling their protein expression. However, their role in OA is less clear. Identifying RBPs in OA is of great importance to better understand OA pathophysiology and to figure out potential targets for OA treatment. Hence, in this manuscript, we summarize the recent knowledge on the role of dysregulated RBPs in OA and hope it will provide new insight for OA study and targeted treatment.

Emerging roles of RNA binding proteins in intervertebral disc degeneration and osteoarthritis

“…137 AS is believed to play an essential role in the regulation of gene diversity associated with the OA pathogenesis. 138,139 Sun et al (2006) demonstrated that RBPMS binds to Smads and increases the expression of Smad2 and Smad3 by enhancing phosphorylation at the C-terminal of Smad2 and Smad3. 140 Smad2 and Smad3 are also involved in maintaining chondrocyte homeostasis through regulation of Col II and ACAN.…”

“…found that expression of RBPMS is positively associated with splicing events in vascular smooth muscle cells, and RBPMS controls other splicing factors, including MBNL1, MBNL2, LSM14B, and Myocardin 137 . AS is believed to play an essential role in the regulation of gene diversity associated with the OA pathogenesis 138,139 . Sun et al (2006) demonstrated that RBPMS binds to Smads and increases the expression of Smad2 and Smad3 by enhancing phosphorylation at the C‐terminal of Smad2 and Smad3 140 .…”