| 研究課題/領域番号 |
26461542
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| 研究種目 |
基盤研究(C)
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| 配分区分 | 基金 |
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| 応募区分 | 一般 |
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| 研究分野 |
小児科学
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| 研究機関 | 浜松医科大学 |
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研究代表者 |
山口 理恵 浜松医科大学, 医学部, 特任研究員 (50420360)
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| 研究期間 (年度) |
2014-04-01 – 2017-03-31
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| 研究課題ステータス |
中途終了 (2016年度)
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| 配分額 *注記 |
4,030千円 (直接経費: 3,100千円、間接経費: 930千円)
2016年度: 1,040千円 (直接経費: 800千円、間接経費: 240千円)
2015年度: 1,430千円 (直接経費: 1,100千円、間接経費: 330千円)
2014年度: 1,560千円 (直接経費: 1,200千円、間接経費: 360千円)
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| キーワード | FGD / NNT deficiency / oxidative stress / mitochodria / bioenergetics / ATP / MAPK pathway / NNT activity / patient / lymphocyte / mitochondria / NNT / ROS / cortisol / redox status / HAC15 cells |
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| 研究実績の概要 |
The objectives of this project are 1) to verify NNT defect impairs cellular redox status and mitochondrial bioenergetics both in vitro and in vivo; 2) to validate the impaired cellular redox status mediates MAPK pathways to inhibit mitochondrial ATP production and induce apoptosis and subsequent decreased cellular viability; 3) to identify new genes responsible for FGD and elucidate the underlying mechanism(s)
The following results were obtained.
1. NNT knockdown resulted in an oxidized cellular redox status and impaired mitochondrial bioenergetics in HAC15 cells (a human adrenocortical cell line)
2. The FGD patient with NNT deficiency showed higher ROS production rate in the lymphocytic mitochondria, suggesting NNT deficiency lead to increased oxidative stress in the patient.
3. The effect of NNT deficiency on mitochondrial bioenergetics in the FGD patient was not performed due to lack of blood sample and all the remaining experiments were stopped due to the researcher’s retirement.
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