Abstract
Osteoporosis (OP) is a highly prevalent chronic disease. The anabolic agent parathyroid hormone (PTH) is often prescribed for the treatment of OP to strengthen bone quality and decrease the risk of fracture, although the specific mechanisms are still unclear. Lysyl oxidase (LOX) can stabilize the organic matrix through catalyzing the cross-linking of collagen and elastin. In this study, we established osteoporotic models via ovariectomizing C57BL/6J mice and treating them with PTH. We further aimed to determine the expression changes of the LOX family, impacted by PTH, in ovariectomized mice. We observed that bone mass was reduced and bone microstructure was deteriorative in ovariectomized mice. And PTH attenuated the microstructural damage and accelerated bone remodeling, as confirmed via μCT and HE staining. Serum levels of copper and zinc indirectly proved the results. The expression levels of five members of the LOX family all declined in ovariectomized mice compared to in sham-operated control mice (p < 0.05), and the daily injection of PTH successfully reversed the low expression of LOXs in OP. The current study examined expression changes of LOXs in osteoporotic mice and PTH-treated osteoporotic mice for the first time, and provided an important piece of evidence that the aberrant expression of LOXs had intimate associations with the occurrence and development of OP. And LOXs may act as the downstream effectors of PTH, contributing to unbalanced bone metabolism and damaged bone microstructure. Consequently, LOXs may act as promising therapeutic targets for OP.