YBX1 Promotes MSC Osteogenic Differentiation by Activating the PI3K/AKT Pathway

Bone metabolism has an essential role in bone disease, but its specific mechanism remains unclear. Y-Box Binding Protein 1 (YBX1) is a gene with broad nucleic acid binding properties, which encodes a highly conserved cold shock domain protein. Previous studies have shown that YBX1 is closely related to cell differentiation. However, the function of YBX1 in osteoblast differentiation of bone marrow mesenchymal stem cells (MSCs) was unclear.

To explore the effect and specific mechanism of YBX1 in osteogenic differentiation of MSCs, we used PCR, Western blot, Alizarin red Staining, alkaline phosphatase (ALP) assays, and siRNA knockdown in our research. We found that YBX1 gradually increased during the process of osteogenic differentiation of MSCs. YBX1 siRNA could negatively regulate the MSCs osteogenic differentiation. Mechanistic studies revealed that YBX1 knockdown could inhibit PI3K/AKT pathway. Furthermore, the specific agonist (SC79) of PI3K/AKT pathway could restore the impaired MSCs osteogenic differentiation which was mediated by YBX1 knockdown. Taken together, we concluded that YBX1 could positively regulate the osteogenic differentiation of MSCs by activating the PI3K/AKT pathway.

These results helped us further understand the mechanism of osteogenesis and revealed that YBX1 might be a selectable target in the bone repair field.

Our study provides a new target and theoretical basis for the treatment of bone diseases.