LOXG473A induces the formation of osteoclasts in RAW264.7 cells via IL-6/JAK2/STAT3 signaling

Formation of osteoclasts is known to be closely associated with osteoporosis progression. LOX is a key enzyme that catalyzes the synthesis of collagen, which is the new mediator in osteoclast formation. However, the effect of LOXG473A on of osteoclast formation needs to be explored. Thereby, we sought to explore the effect of LOXG473A on formation of osteoclasts and its underlying mechanism. To investigate the function of LOXG473A in osteoclast formation, Raw264.7 cells were stably transfected with LOX-WT or LOX-MUT (LOXG473A). Real-time PCR and western blotting were used to detect the relative levels of osteoclast formation related genes and proteins. TRAP staining and immunofluorescence staining were used to test the ability of Raw264.7 cells to form osteoclasts and the ability of cells to form rings, respectively. Bone erosion assay was used to test bone resorptive activity. The data indicated that LOXG473A significantly enhanced the ability of osteoclasts forming, ring-forming and bone resorpting in Raw264.7 cells. Mechanically, LOXG473A upregulated the expressions of NFATC1, ACP5, CTSK, IL-6, and the proportion of p-JAK2/JAK2 and p-STAT3/STAT3, thereby promoting the formation of osteoclasts. In conclusion, we have verified that LOXG473A induces the proliferation of osteoclasts in Raw264.7 cells via IL-6/ JAK2/STAT3 signaling, suggesting a novel strategy for studying osteoporosis.

Automated summary

The study showed that LOXG473A significantly enhances the formation, ring formation, and bone resorptive activity of osteoclasts, promoting their proliferation through the IL-6/JAK2/STAT3 signaling pathway.