Hatch Nan E, Nociti Francisco, Swanson Erica, Bothwell Mark, Somerman Martha
Department of Physiology and Biophysics, University of Washington, Seattle, Washington 98195, USA.
Connect Tissue Res. 2005;46(4-5):184-92. doi: 10.1080/03008200500237203.
Fibroblast growth factor/fibroblast growth factor receptor (FGF/FGFR) signaling has been linked to the aberrant mineralization phenotype of craniosynostosis syndromes. One critical aspect of mineralization involves the elaboration and transport of pyrophosphate into the extracellular matrix with subsequent enzymatic hydrolysis into phosphate. Altered expression of the pyrophosphate elaborating factors, TNAP (tissue nonspecific alkaline phosphatase), PC-1, and ANK, downstream of FGF/FGFR signaling may provide a potential mechanism for the craniosynostosis phenotype. As an initial step toward testing this hypothesis, we confirmed that ANK mRNA is upregulated during osteoblast differentiation in culture. Subsequently, the effect of FGF2 treatment on expression of PC-1, ANK, and TNAP in the calvarial osteoblastic cell line, MC3T3E1(C4), was investigated. FGF2 specifically induced expression of PC-1 and ANK while inhibiting expression of TNAP, at both mRNA and protein levels. Concordant with these changes in gene expression, FGF2 inhibited mineralization. These results suggest that FGF/FGFR signaling may affect mineralization via changes in the elaboration and metabolism of pyrophosphate.
成纤维细胞生长因子/成纤维细胞生长因子受体(FGF/FGFR)信号传导与颅缝早闭综合征的异常矿化表型有关。矿化的一个关键方面涉及焦磷酸盐向细胞外基质的合成与转运,随后被酶水解为磷酸盐。FGF/FGFR信号传导下游的焦磷酸盐合成因子,即组织非特异性碱性磷酸酶(TNAP)、PC-1和ANK的表达改变,可能为颅缝早闭表型提供了一种潜在机制。作为检验这一假设的第一步,我们证实了在培养的成骨细胞分化过程中ANK mRNA上调。随后,研究了FGF2处理对颅骨成骨细胞系MC3T3E1(C4)中PC-1、ANK和TNAP表达的影响。FGF2在mRNA和蛋白质水平上均特异性诱导PC-1和ANK的表达,同时抑制TNAP的表达。与这些基因表达变化一致,FGF2抑制矿化。这些结果表明,FGF/FGFR信号传导可能通过焦磷酸盐的合成与代谢变化来影响矿化。