| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Outline of Final Research Achievements |
SOD (Superoxide dismutase) is an enzyme that alternately catalyzes the dismutation of the superoxide (O2－) radical into either ordinary molecular oxygen (O2) or hydrogen peroxide (H2O2). Thus, SOD is an important antioxidantdefense in nearly all living cells exposed to oxygen. We generated DMP1 cre SOD2 KO mice and conditionally inactivated SOD2 in osteocytes and odontoblasts. We found that loss of SOD2 enhanced thickness of cementum in teeth. In the other hands, periodontal ligament and alveolar bone in DMP1 cre SOD2 KO mice were normal compared with wild type mice. Overexpression of SOD2 in cementoblasts decreased the expression of DMP1 and CP23, which were differentiation markers of cementum. On the contrary, knockdown of SOD2 using siRNA increased both proliferation and differentiation in cementoblasts. These data suggested that SOD2 supressed proliferation and differentiation in cementoblasts.
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