| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 2005: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2004: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2003: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Research Abstract |
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.
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