| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Outline of Final Research Achievements |
Blood levels of selenoprotein P (SeP) are elevated in patients with type 2 diabetes. Also concentration of SeP correlated with insulin resistance. In this study, we aimed to clarify how excess selenoprotein P (SeP) induces disorder of MIN6 cells, a model of pancreatic beta cells. SeP induced cell death in dose-dependent manner in MIN6 cells. SeP induced caspase-3 activation and pan caspase inhibitor z-VAD-FMK rescued SeP-induced cell death suggested that excess SeP induces apoptosis in MIN6 cells. Several reports were shown the relationship between ER-stress and diabetes, in the next series of experiments we focused on contribution of ER-stress on SeP-dependent apoptosis. Marker proteins of endoplasmic reticulum (ER) stress such as CHOP and GRP78 were also induced by SeP. SeP-induced cell death were abolished by 4-Phenylbutyric acid, an inhibitor of ER stress. These result suggested that excess amount of SeP induced apoptosis via ER stress in pancreatic beta cells.
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