PALLADIN regulates osteogenic differentiation of bone marrow mesenchymal stem cells and protects against bone loss in ovariectomized mice.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Osteoporosis is a systemic skeletal disease associated with reduced bone density and impaired bone quality, which leading to a greater risk of fracture. The pathogenesis of osteoporosis is closely associated with compromised osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). The actin-cytoskeleton associated protein PALLADIN has been reported to play a central role in the remodeling of the actin-cytoskeleton. However, no studies to date have established whether PALLADIN can influence osteogenic differentiation of BMSCs or the onset of osteoporosis. Here, PALLADIN knockdown was observed to reduce osteogenic differentiation of BMSCs, confirming the involvement of the gene in osteoporosis. Knockdown also altered the cytoskeletal organization and reduced Ras homolog family member A (RhoA) activity to inhibit osteogenic differentiation. The results of the in vivo experiments showed that overexpression of Palladin reversed bone loss and marrow adipose tissue (MAT) accumulation in OVX mice, while Palladin knockdown increased both bone loss and MAT accumulation in OVX mice. Together, these results suggest a model in which Palladin protects against bone loss induced by OVX through the promotion of BMSCs osteogenesis. In human osteoporotic BMSCs, PALLADIN expression is significantly downregulated, correlating with disease status. While functional validation in prim

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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