Research of apoptosis induction by LPS and heat stress for pulp regeneration therapy

最近，我们在体内证明了热应激诱导的牙髓细胞凋亡与牙髓细胞增殖和分化之间的关系，以促进牙髓创伤愈合过程中的牙髓再生(J.Dent)。Res.，2001；J.Dent.Res.，2003；Oper.登特，2003；J.Endod。2003年)。我们还证明了热应激下的牙髓细胞表现出凋亡和耐热性，热应激后存活的牙髓细胞吞噬了凋亡的牙髓细胞(J.Cell Biochem，2005)。进一步，我们研究了牙髓细胞对内毒素和热应激的影响，发现内毒素通过在内毒素和热应激下对牙髓细胞HSF1、HSP27、AKT和NF-κB/IκBα的修饰和激活而对牙髓细胞产生独特的影响。此外，我们还观察了低氧对牙髓细胞凋亡和细胞周期停滞的影响，发现低氧通过调节p21、细胞周期蛋白D2、Rb和P53诱导牙髓细胞周期停滞和凋亡。

Recently, we demonstrated the in vivo relationship between pulp apoptosis induced by heat stress and pulp cell proliferation and differentiation for pulp regeneration during pulp wound healing (J. Dent. Res., 2001 ; J. Dent. Res., 2003 ; Oper. Dent., 2003 ; J. Endod. 2003). We also demonstrated that pulp cells exposed to heat stress show apoptosis and the thermo-tolerance, and that the survived pulp cells after heat stress phagocytose apoptotic pulp cells (J. Cell Biochem, 2005). Further, we examined the effects of sequential exposure of pulp cells to LPS and heat stress, and found that LPS has the unique effects on pulp cells through the modification and activation of HSF1, HSP27, Akt, and NF-κB/IκBα during sequential exposure to LPS and heat stress. Also, we examined the effects of hypoxia on pulp cell apoptosis and cell cycle arrest, and found that the cell cycle arrest and apoptosis was induced on pulp cells by hypoxia through the regulation of p21, cyclin D2,Rb, andp53.