Ben Lagha N, Menuelle P, Seurin D, Binoux M, Lebouc Y, Berdal A
Laboratoire de Biologie-Orofaciale et Pathologie, INSERM EMI U-0110, Université Paris 7, IFR 58, Institut Biomédical des Cordeliers, Esc. E, 2è ét., 15-21 rue de l'Ecole de Médecine, 75270 Paris, France.
Connect Tissue Res. 2002;43(2-3):515-9.
In humans, intrauterine growth retardation (hIUGR) is correlated with an overexpression of insulin-like growth factor binding protein 1 (IGFBP-1). The affected children also present a delay in bone mineralization. In this study, transgenic 12-day-old mutant mice overexpressing human IGFBP-1 hepatospecifically showed a severe growth retardation. Alcian blue and alizarin red S staining of the skeleton revealed mineralization defects at the posterior level of the skull (delayed suture closure) and in appendicular and axial skeleton. Furthermore, microradiographic analysis showed a reduced bone density in the same areas. Thus, overexpressing of hIGFBP-1 demonstrates early postnatal life growth retardation and a delay in mineralization in transgenic mutant mice. These data show the involvement of the IGF/IGFBP system and more particularly IGFBP-1 in the biomineralization process.
在人类中，宫内生长迟缓（hIUGR）与胰岛素样生长因子结合蛋白1（IGFBP-1）的过表达相关。受影响的儿童还存在骨矿化延迟的情况。在本研究中，肝特异性过表达人IGFBP-1的12日龄转基因突变小鼠表现出严重的生长迟缓。骨骼的阿尔新蓝和茜素红S染色显示，在颅骨后部水平（缝线闭合延迟）以及附属骨骼和中轴骨骼存在矿化缺陷。此外，显微放射照相分析显示相同区域的骨密度降低。因此，hIGFBP-1的过表达证明转基因突变小鼠出生后早期生长迟缓以及矿化延迟。这些数据表明IGF/IGFBP系统，尤其是IGFBP-1参与了生物矿化过程。
