The widespread application of hormones leads to steroidal osteonecrosis and BMSCs have important roles in treating steroidal osteonecrosis. Mir-1301 involves in several diseases. However, Mir-1301’s effect on BMSCs proliferation and osteogenic differentiation in hormonal osteonecrosis
has not been elucidated. Rat BMSCs were isolated and assigned into control groups; Dex group (1μM dexamethasone was added); Mir-1301 group and si-Mir-1301 group followed by analysis of miR-1301 and SOX11 level by Real time PCR, cell proliferation by MTT assay, Caspase3 activity kit,
OPN and Runx2 expression by Real time PCR, and ALP activity. Under hormone treatment, Mir-1301 expression in BMSCs cells was significantly increased, proliferation was inhibited, Caspase3 activity was increased, SOX11, OPN and Runx2 expression was decreased and ALP activity was reduced (P
<0.05). The above changes were more significant after transfection of Mir-1301 mimics (P <0.05). The addition of Mir-1301 inhibitor to Dex-treated BMSCs could down-regulate Mir-1301, significantly increase the expression of SOX11, OPN and Runx2, promote cell proliferation, decrease
Caspase3 activity and increase ALP activity (P <0.05). The target gene of Mir-1301 is SOX11. Mir-1301 expression in BMSCs cells is increased during steroid-induced osteonecrosis. Down-regulating Mir-1301 during steroid-induced osteonecrosis can inhibit BMSCs apoptosis and promote
proliferation and osteogenesis via targeting SOX11.