| Objective: C-type natriuretic peptide(CNP)is believed to be produced locally in the kidneys and possess several renoprotective properties.In contrast,Fibroblast growth factor(FGF)-23 elevates in the early stage of chronic kidney disease(CKD)and predicts its outcomes.Currently,several studies have demonstrated that CNP and FGF-23 act through a close pathway,and moreover,FGF-23/mitogen-activated protein kinase(MAPK)can be obviously suppressed by CNP.Methods: In the present study,human mesangial cells(MCs)were incubated in serum-containing medium in the absence or presence of CNP(0,10 and 100 pm)for 24,48 and 72 h,respectively.Results: CNP administration significantly suppresses MCs proliferation in a time-and dose-dependent manner.As a down-stream signaling of CNP activation,the expressions of natriuretic peptide receptor(NPR)-B,cyclic guanosine monophosphate-dependent protein kinases II and NPR-C were obviously augmented,whereas neutral endopeptidase expression was significantly decreased after CNP treatment in MCs.FGF-23,FGF receptor-1 and RAF-1 experienced a pronounced down-regulation in MCs with different doses of CNP throughout the whole observational period.Conclusion: CNP may dampen FGF-23 expression via MAPK signaling pathway in MCs. |