Protective effect of estrogen against calcification in the cartilage endplate.

Clinical studies report that endogenous estrogen depletion is associated with disc degeneration. The present study aimed to investigate the effect and mechanism of estrogen on disc degeneration of the cartilage endplate. Three groups of mice with bilateral ovariectomy + 17β-estradiol injection (OVX + E2 Group), bilateral ovariectomy + vehicle injection (OVX + vehicle), or sham operation + vehicle injection (Sham Group) were included in this study. The mice were sacrificed at 12 weeks and the cartilage endplate (CEP) were harvested. The calcification status was evaluated by Alizarin red staining and RT-PCR, which demonstrated the calcification level of the CEP gradually developed from the Sham Group, OVX + E2, to the OVX + vehicle group. The CEP cells were isolated, cultured, and treated with IL-1β (75 ng/ml) for 24 h, with or without a pretreatment of 17β-E2 for 1 h. RT-PCR analysis of calcification-related genes ALP, OCN, RUNX2, and COL-I were analyzed, and calcification of CEP cells induced by IL-1β was reversed by pretreatment with 17β-E2, in a dose-dependent manner. The protective effect of 17β-E2 was abolished by estrogen receptor antagonist ICI182,780. These results suggest that decreased estrogen level may accelerate degeneration of the cartilage endplate by increasing calcification, which may be induced by IL-1β, in a dose-dependent manner. IJCEP