DUSP10调控c-Fos/NFATc1信号通路抑制破骨细胞分化研究OA

[Objective]To investigate the regulatory role of DUSP10 in osteoclast differentiation and its molecular mechanism.[Methods]RAW264.7 cells were used as a model and divided into three groups:the NC group(untreated cells),the DUSP10-NC group(transfected with empty plasmid),and the DUSP10-OE group(transfected with DUSP10 overexpression plasmid),DUSP10-sh group(transfected with DUSP10 interference plasmid).Cell viability was assessed via CCK-8 assay,osteoclast differentiation was evaluated by TRAP staining,and protein expression levels of c-Fos,NFATc1,and TRAP were measured using Western blot.[Results]Overexpression of DUSP10 significantly inhibited osteoclast viability(P＜0.05),reduced the number of TRAP-positive cells(P＜0.05),and downregulated c-Fos,NFATc1,and TRAP protein expression(P＜0.005).Conversely,inhibition of DUSP10 promoted osteoclast differentiation(P＜0.05)and upregulated the expression of the aforementioned proteins.[Conclusion]DUSP10 suppresses osteoclast differentiation by inhibiting the c-Fos/NFATc1 signaling pathway,providing a novel theoretical basis for targeted therapies for bone metabolic disorders such as osteoporosis.