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碱性成纤维细胞生长因子通过抑制破骨细胞分化因子的产生,抑制1α,25 - 二羟基维生素D(3)诱导的破骨细胞形成。

Basic fibroblast growth factor inhibits osteoclast formation induced by 1alpha,25-dihydroxyvitamin D(3) through suppressing the production of osteoclast differentiation factor.

作者信息

Nakagawa N, Yasuda H, Yano K, Mochizuki S i, Kobayashi N, Fujimoto H, Yamaguchi K, Shima N, Morinaga T, Higashio K

机构信息

Research Institute of Life Science, Snow Brand Milk Products Co. Ltd. , Tochigi, 329-0512, Japan.

出版信息

Biochem Biophys Res Commun. 1999 Nov;265(1):45-50. doi: 10.1006/bbrc.1999.1621.

Abstract

Basic fibroblast growth factor (bFGF) inhibited osteoclast-like cell (OCL) formation in cocultures of mouse spleen cells with either osteoblasts or a stromal cell line, ST2, in the presence of 1alpha, 25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)]. bFGF directly acted on osteoblasts/stromal cells, but not osteoclast progenitors, to inhibit 1,25(OH)(2)D(3)-induced OCL formation. bFGF suppressed the mRNA expression of osteoclast differentiation factor (ODF) but did not affect that of osteoclastogenesis inhibitory factor (OCIF) in ST2 cells treated with 1,25(OH)(2)D(3) and dexamethasone. Enzyme-linked immunosorbent assay showed that bFGF hardly affected OCIF production in the treated ST2 cells. A genetically engineered soluble form of ODF, but not anti-OCIF neutralizing antibody, abolished bFGF-mediated inhibition of OCL formation. bFGF suppressed the binding of (125)I-labeled OCIF to both ST2 cells and osteoblasts treated with 1,25(OH)(2)D(3). These findings indicate that bFGF inhibits 1,25(OH)(2)D(3)-induced OCL formation via suppression of ODF production by osteoblasts/stromal cells.

摘要

在1α,25 - 二羟基维生素D(3)[1,25(OH)₂D₃]存在的情况下,碱性成纤维细胞生长因子(bFGF)在小鼠脾细胞与成骨细胞或基质细胞系ST2的共培养体系中抑制破骨细胞样细胞(OCL)的形成。bFGF直接作用于成骨细胞/基质细胞,而非破骨细胞前体细胞,以抑制1,25(OH)₂D₃诱导的OCL形成。bFGF抑制了破骨细胞分化因子(ODF)的mRNA表达,但不影响用1,25(OH)₂D₃和地塞米松处理的ST2细胞中破骨细胞生成抑制因子(OCIF)的mRNA表达。酶联免疫吸附测定表明,bFGF对处理后的ST2细胞中OCIF的产生几乎没有影响。一种基因工程可溶性形式的ODF,而非抗OCIF中和抗体,消除了bFGF介导的对OCL形成的抑制作用。bFGF抑制了¹²⁵I标记的OCIF与用1,25(OH)₂D₃处理的ST2细胞和成骨细胞的结合。这些发现表明,bFGF通过抑制成骨细胞/基质细胞产生ODF来抑制1,25(OH)₂D₃诱导的OCL形成。

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