| Project/Area Number |
24390421
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pathobiological dentistry/Dental radiology
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| Research Institution | Nagasaki University |
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Principal Investigator |
NAKAMURA Takashi 長崎大学, 医歯薬学総合研究科(歯学系), 教授 (30172406)
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| Co-Investigator(Kenkyū-buntansha) |
SUMI Misa 長崎大学, 医歯薬学総合研究科(歯学系), 准教授 (90284702)
HOTOKEZAKA Yuka 長崎大学, 病院(歯学系), 講師 (10244089)
SASAKI Miho 長崎大学, 病院(歯学系), 助教 (10437874)
KATAYAMA Ikuo 長崎大学, 医歯薬学総合研究科(歯学系), 助教 (80295089)
TASHIRO Shigeki 長崎大学, 病院(医学系), 助教 (20300882)
ICHIKAWA Youko 長崎大学, 病院(歯学系), 助教 (90380857)
角 忠輝 長崎大学, 医歯(薬)学総合研究科, 准教授 (80284701)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥18,200,000 (Direct Cost: ¥14,000,000、Indirect Cost: ¥4,200,000)
Fiscal Year 2014: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥8,450,000 (Direct Cost: ¥6,500,000、Indirect Cost: ¥1,950,000)
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| Keywords | アポトーシス / 非アポトーシス / cPLA2 / ｃPLA2 / knock-outマウス |
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| Outline of Final Research Achievements |
Our study evaluated the role of cytosolic phospholipase A2 (cPLA2) in the mechanisms of various cell death, including apoptosis, necroptosis, and autophagy. We obtained.the following results:(1) We have established a cPLA2-/- mouse lung embryonal fibroblast cell line from the CKO-cPLA2-/- mice.(2) We found that hypoxic and DNA damaging stresses trigger a common endoplasmic reticulum (ER) stress response and unfolded protein response (UPRs) signalling pathway leading to apoptotic cell death. Also, we found that autophagic in addition to apoptotic cell death occurs in the cells exposed to the external stresses. (3) The results obtained during this study suggested that plasma membrane-associated proteins such as mucin-1 (MUC1) and phosphatidylinositol-3-kinase (PI3K)/Akt/glycogen synthase kinase-3β (GSK-3β) complexes may play a critical role in the ER stress and UPR signalling pathway in dying cells.
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