Kameda T, Miyazawa K, Mori Y, Yuasa T, Shiokawa M, Nakamaru Y, Mano H, Hakeda Y, Kameda A, Kumegawa M
Department of Orthodontics, School of Dentistry at Niigata, Nippon Dental University, Japan.
Biochem Biophys Res Commun. 1996 Mar 27;220(3):515-9. doi: 10.1006/bbrc.1996.0436.
In contrast to vitamin K1(VK1), vitamin K2(VK2) inhibited osteoclastic bone resorption by unfractionated bone cells and isolated osteoclasts. To investigate the mechanism of inhibition of osteoclastic bone resorption by VK2, we examined the effect of this vitamin on osteoclast apoptosis using a DNA-binding fluorescent dye, Hoechst 33258. In unfractionated bone cells and isolated osteoclasts on dentin slices, we first demonstrated that VK2 induced osteoclast apoptosis, but VK1 did not. Moreover, cycloheximide inhibited VK2-induced osteoclast apoptosis. These results suggest the possibility that VK2 inhibits osteoclastic bone resorption by targeting osteoclasts to undergo apoptosis, which leads to cell death.
与维生素K1(VK1)不同,维生素K2(VK2)可抑制全部分离骨细胞和分离破骨细胞的破骨细胞性骨吸收。为了研究VK2抑制破骨细胞性骨吸收的机制,我们使用一种DNA结合荧光染料Hoechst 33258检测了该维生素对破骨细胞凋亡的影响。在牙本质切片上的全部分离骨细胞和分离破骨细胞中,我们首先证明VK2可诱导破骨细胞凋亡,而VK1则不能。此外,放线菌酮可抑制VK2诱导的破骨细胞凋亡。这些结果提示,VK2可能通过靶向破骨细胞使其发生凋亡,进而导致细胞死亡,从而抑制破骨细胞性骨吸收。