In vivo and in vitro comparison of the effects of FGF-2 null and haplo-insufficiency on bone formation in mice

被引：55

作者：

Naganawa, T

Mao, L

Abogunde, E

Sobue, T

Kalajzic, I

Sabbieti, M

Agas, D

Hurley, MM ^{[1
]}

机构：

[1] Univ Connecticut, Ctr Hlth, Dept Med, Farmington, CT 06030 USA

[2] Univ Connecticut, Ctr Hlth, Dept Genet & Dev Biol, Farmington, CT 06030 USA

[3] Univ Camerino, I-62032 Camerino, Italy

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2006年 / 339卷 / 02期

关键词：

fibroblast growth factor-2; gene; haplo-insufficiency; mice; bones; DEXA; FGF receptor2; Runx2;

D O I：

10.1016/j.bbrc.2005.10.215

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

We previously reported that deletion of the Fgf2 gene (Fgf2-/-) resulted in decreased bone mass in adult mice. This study examines the effect of haplo-insuffiency (Fgf2+/-) on bone loss in vertebrae from these mutant mice. Fgf2+/+ mice attained peak bone mass at 89 months of age. In contrast BMD was significantly reduced in vertebrae from adult (8-9) Fgf2+/- mice. Exogenous FGF-2 rescued reduced bone nodule formation in Fgf2+/- and Fgf2-/- cultures. Runx2 mRNA was reduced in cultures from Fgf2+/- and Fgf2-/- mice. FGF receptor2 mRNA and protein were markedly reduced in Fgf2+/- and Fgf2-/- mice. Decreased bone formation in Fgf2 mutant mice may correlate with impaired FGFR signaling, decreased Runx2 gene expression. (c) 2005 Elsevier Inc. All rights reserved.

引用

页码：490 / 498

页数：9

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