The role of growth factors on wound healing of maxillofacial bone

机械应力影响骨创伤愈合的分子基础尚未得到很好的研究。局部产生的自分泌或旁分泌因子调节伤口愈合过程。碱性成纤维细胞生长因子在这一过程中起着重要的作用。我们在这里展示了bFGFF的新发现，成纤维细胞生长因子-2(FGF-2)被认为间接刺激骨形成和吸收。我们研究了对成熟破骨细胞的直接作用。成纤维细胞生长因子-2(10-11M)在兔破骨细胞分离培养中对凹陷的形成有最大刺激作用(1.9倍)，而在骨细胞混合培养中，成纤维细胞生长因子-2(10-9M)的刺激作用是7.5倍。成纤维细胞生长因子-2上调了包括p42/p44丝裂原活化蛋白(MAP)在内的细胞蛋白的磷酸化，并增加了成纤维细胞生长因子受体-1的激酶活性。这些结果提示，成纤维细胞生长因子-2通过激活成纤维细胞生长因子受体-1和p42/p44蛋白激酶，直接作用于成熟破骨细胞，在生理或病理浓度下刺激骨吸收。

Molecular basis of wound healing of bone affected by mechanical stress has not been studied well. Locally produced autocrine or paracrine factors regulate the wound healing process. Basic fibroblast growth factor (bFGF) has the potent effects on this process. We have shown here the new findings of bFGF.Fibroblast growth factor-2 (FGF-2) is known to stimulate bone formation and resorption indirectly. We investigated the direct action of on mature osteoclasts. FGF-2 (10-11M) exhibited maximum stimulation (1.9-fold) of pit formation in isolated rabbit osteoclast cultures, whereas in mixed cultures of bone cells, FGF-2 (10-9M) showed the 7.5-fold stimulation. FGF-2 up-regulated the phosphorylation of cellular proteins including p42/p44 mitogen-activated protein (MAP) kinase, and increased the kinase-activity of FGF receptor-1. These results suggest that FGF-2 acts directly on mature osteoclasts through activation of FGF receptor-1 and p42/p44 MAP kinase, causing the stimulation of bone resorption at physiological or pathological concentrations.