| Project/Area Number |
22591142
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | Kurume University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
POVALKO Nataliya 久留米大学, 医学部, 准教授 (10399181)
NISHIOKA Junko 久留米大学, 医学部, 助教 (00449919)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | ミトコンドリア / 電子伝達系酵素 / 老化 / 複合体II / エネルギー産生系異常 / Klotho遺伝子 / KOマウス / 早老症 / Ｋｌｏｔｈｏ遺伝子 / ＫＯマウスモデル / klotho遺伝子 / エネルギー代謝 / ミトコンドリアDNA |
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| Research Abstract |
Premature aging model (klotho, kl-/-) and natural aged (CD-1) mice were used to compare the mitochondrial energy metabolism and morphometrical property in kidney and brain. Natural aged mice tended to renal hypertrophy with decreasing glomerulus and decreased the total protein content, oxygen consumption and respiratory chain enzyme activities, complex I, II, I-III, II-III, and IV, in renal mitochondria. Klotho mice had contracted kidney with decreasing normal glomerulus and decreased oxygen consumption with increasing the total protein content, however the most respiratory chain enzyme activities retained in renal mitochondria. Klotho mice reduced only complex II and I-III activities. In endbrain, Natural aged mice had hypertrophic mitochondria with numerical decreasing and tend to decrease oxygen consumptions and respiratory chain enzyme activities in synaptosome and synaptosomal mitochondria. Klotho mice had atrophy of the cerebrum with abnormal distribution of neuronal cellsin cerebral cortex layers, mortar region, and with atrophic mitochondria. Klotho mice preserved the oxygen consumptions and the respiratory chain enzyme activities, only reducing complex II activity, with increasingtotal protein contents in synaptosome and synaptosomal mitochondria. Klotho mouse defected klotho gene expression causes the mitochondrial dysfunction in kidney and brain to change some morphological properties with similarities to natural aging mouse. However, the dysfunction and the morphometrical properties make some differences with the natural aging mice. It is indicated that klotho mouse induce mitochondrial dysfunction by abnormal proteins accumulation affected to neuronalmigration that cerebral growth retardation occur for premature aging model.
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