Song Insun, Jeong Byung-Chul, Choi Yong Jun, Chung Yoon-Sok, Kim Nacksung
Shool of Biological Sciences, Seoul National University, Seoul 08826, Korea.
Departments of Pharmacology and Biomedical Sciences, Chonnam National University Medical School, Gwangju 61469, Korea.
BMB Rep. 2016 Jun;49(6):343-8. doi: 10.5483/bmbrep.2016.49.6.032.
GATA4 has been reported to act as a negative regulator in osteoblast differentiation by inhibiting the Dlx5 transactivation of Runx2 via the attenuation of the binding ability of Dlx5 to the Runx2 promoter region. Here, we determine the role of GATA4 in the regulation of bone sialoprotein (Bsp) in osteoblasts. We observed that the overexpression of Runx2 or Sox9 induced the Bsp expression in osteoblastic cells. Silencing GATA4 further enhanced the Runx2- and Sox9-mediated Bsp promoter activity, whereas GATA4 overexpression down-regulated Bsp promoter activity mediated by Runx2 and Sox9. GATA4 also interacted with Runx2 and Sox9, by attenuating the binding ability of Runx2 and Sox9 to the Bsp promoter region. Our data suggest that GATA4 acts as a negative regulator of Bsp expression in osteoblasts. [BMB Reports 2016; 49(6): 343-348].
据报道,GATA4通过减弱Dlx5与Runx2启动子区域的结合能力,抑制Dlx5对Runx2的反式激活作用,从而在成骨细胞分化中作为负调节因子发挥作用。在此,我们确定GATA4在成骨细胞中对骨唾液酸蛋白(Bsp)调控中的作用。我们观察到,Runx2或Sox9的过表达诱导成骨细胞中Bsp的表达。沉默GATA4进一步增强了Runx2和Sox9介导的Bsp启动子活性,而GATA4过表达则下调了Runx2和Sox9介导的Bsp启动子活性。GATA4还通过减弱Runx2和Sox9与Bsp启动子区域的结合能力,与Runx2和Sox9相互作用。我们的数据表明,GATA4在成骨细胞中作为Bsp表达的负调节因子发挥作用。[《BMB报告》2016年;49(6): 343 - 348]