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

最近，我们证明了热应激诱导的髓细胞凋亡与髓外伤愈合过程中髓细胞增殖和分化的体内关系(J. Dent。Res., 2001；j .凹痕。Res., 2003；③。凹痕。， 2003；J. endd . 2003)。我们还证明，暴露于热应激的髓细胞表现出凋亡和耐热性，并且存活的髓细胞在热应激后吞噬凋亡的髓细胞（J. Cell Biochem, 2005）。进一步，我们研究了连续暴露于LPS和热应激对牙髓细胞的影响，发现LPS在连续暴露于LPS和热应激时通过修饰和激活HSF1、HSP27、Akt和NF-κB/ i -κB α对牙髓细胞具有独特的作用。此外，我们还研究了缺氧对髓细胞凋亡和细胞周期阻滞的影响，发现缺氧通过调控p21、cyclin D2、Rb和p53诱导髓细胞周期阻滞和细胞凋亡。

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.