| Project/Area Number |
06833018
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
老化(加齢)
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| Research Institution | Tokyo Metropolitan Institute of Gerontology |
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Principal Investigator |
FUJITA Toshiko Tokyo Metropolitan Institute of Gerontology, Mol.Biology, Assistant Researcher, 分子生物学部門, 助手 (00100131)
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| Co-Investigator(Kenkyū-buntansha) |
MARUYAMA Naoki Tokyo Metropolitan Institute of Gerontology, Mol.Pathology, Head, 分子病理部門, 部長 (00115940)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1995: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1994: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | Aging / Senescence / Senescence Marker Protein-30 (SMP30) / Lead Nitrate / Regucalcin / Calcium-Binding Protein / Liver / Carbon Tetrachloride / Nafenopin / Phenobarbital / 遺伝子発現 |
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| Research Abstract |
We reported a novel liver protein, the amounts of which decreased androgen-independently with aging.We designated this protein as senescence marker protein-30 (SMP30) .We have isolated rat and hunan cDNA clones encoding SMP30.SMP30 is a calcium binding protein also called regucalcin which plays a role in the regulation of various enzymes by regulating calcium ions in hepatocytes.It was suggested that the decrease of SMP30 with aging may lead to senile changes in the calcium signaling system of aged livers.The amount of SMP30 in the liver was relatively large (2%) and the deduced amino acid sequence of human SMP30 showed a remarkable homology with that of rat SMP30(89% similarity).The results of genomic Southerm hybridization also indicated the strong evolutionary conservation of SMP30 gene among higher animals.These results support the potentially critical role of SMP30 in tissue specific biological functions of the liver and kidney.SMP30 is exclusively expressed in hepatocytes and renal proximal tubular epitheliums, both of which show high activity of metabolism and transportation.In this study, to elucidate the physiological function of SMP30, we repout the examination of the SMP30 expression in the compensatory hepatocyte proliferation and direct hyperplasia after treatments of two different types of stimulants.Both experimental conditions involve in vivo inductions of liver cell proliferation and liver cell death.SMP30 was isduced by both of proliferative stimuli.However, these inductions were not correlated with DNA synthesis nor mitosis.These results implies that SMP30 is up-regulated in hepatocytes after the proliferative stimuli, but not associated with DNA synthesis and mitosis.Next, we examined the effect of phenobarbital which is a very strong inducers of detoxifying system enzymes.The results suggest that SMP30 is not involved in phase-I enzymes of the drug metabolic system.
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