RBMS3 delays disc degeneration by inhibiting Wnt/β-catenin signaling pathway

Area of Science:

• Biochemistry
• Cell Biology
• Orthopedics

Background:

• Intervertebral disc degeneration is a complex process associated with cellular dysfunction.
• The Wnt/β-catenin signaling pathway plays a critical role in the pathogenesis of disc degeneration.
• Understanding the molecular regulators of nucleus pulposus cell function is crucial for developing therapeutic strategies.

Purpose of the Study:

• To investigate the role of RBMS3 (RNA Binding Protein Splicing Regulator 3) in nucleus pulposus cells.
• To determine the effect of RBMS3 on the Wnt/β-catenin signaling pathway.
• To explore RBMS3 as a potential therapeutic target for intervertebral disc degeneration.

Main Methods:

• Quantified RBMS3 expression in human nucleus pulposus tissues with varying degeneration degrees.
• Utilized recombinant human IL-1β to induce nucleus pulposus cell degeneration in vitro.
• Employed Wnt/β-catenin pathway inhibitors and cell transfection to elucidate RBMS3's mechanism of action.

Main Results:

• RBMS3 expression inversely correlated with the degree of disc degeneration.
• IL-1β treatment decreased RBMS3 expression in nucleus pulposus cells.
• RBMS3 overexpression enhanced cell proliferation, reduced apoptosis and inflammation, and suppressed Wnt/β-catenin signaling (β-catenin, c-myc).

Conclusions:

• RBMS3 plays a protective role in nucleus pulposus cells.
• RBMS3 inhibits the Wnt/β-catenin signaling pathway, thereby mitigating disc degeneration.
• RBMS3 represents a potential therapeutic target for delaying intervertebral disc degeneration.