Department of Pediatrics, the First Affiliated Hospital of Anhui Medical University, Hefei, PR China.
Department of Pediatrics, the First Affiliated Hospital of Anhui Medical University, Hefei, PR China.
Adv Med Sci. 2021 Mar;66(1):206-214. doi: 10.1016/j.advms.2021.03.003. Epub 2021 Mar 15.
Several studies have demonstrated that C-type natriuretic peptide (CNP) stimulates osteoblastic proliferation seemly via antagonizing the expression of fibroblast growth factor (FGF)-23 in vitro. The main aim of the present study is to probe whether the post-receptor pathways of FGF-23 participate in osteogenesis caused by CNP.
Osteoblasts were cultured in the absence or presence of CNP: 0, 10, and 100 pmol/L, for 24 h, 48 h and 72 h, respectively.
The findings of the present study indicated that osteoblastic proliferation was directly promoted by exogenous CNP in a dose-dependent manner; osteoblastic FGF-23 was significantly down-regulated by CNP at 24 h post-treatment; RAF-1, extracellular signal-regulated kinases (ERK), and P38 were substantially suppressed by CNP in a dose- and time-dependent manner; and signal transducer and activator of transcription (STAT)-1 was not changed on the premise of the down-regulated FGF-23 in osteoblasts treated with CNP.
CNP may promote osteogenesis via inhibiting ERK and P38, rather than STAT-1, in the downstream of FGF-23/RAF-1 pathway.
多项研究表明，C 型利钠肽（CNP）似乎通过拮抗成纤维细胞生长因子（FGF）-23 在体外表达来刺激成骨细胞增殖。本研究的主要目的是探究 FGF-23 的受体后途径是否参与 CNP 引起的成骨作用。
分别用浓度为 0、10 和 100 pmol/L 的 CNP 处理成骨细胞 24、48 和 72 h。
本研究结果表明，外源性 CNP 以剂量依赖的方式直接促进成骨细胞增殖；CNP 在处理 24 h 后可显著下调成骨细胞 FGF-23；CNP 以剂量和时间依赖的方式显著抑制 RAF-1、细胞外信号调节激酶（ERK）和 P38；在 CNP 处理的成骨细胞中，FGF-23 下调的前提下，信号转导和转录激活因子（STAT）-1 没有改变。
CNP 可能通过 FGF-23/RAF-1 通路的下游 ERK 和 P38 而不是 STAT-1 来促进成骨作用。
