Effects of Cell Proliferation and Cell Death on the Expression of Sunescence Marker Protein-30 (SMP30) in the Rat Liver.

细胞增殖和细胞死亡对大鼠肝脏中太阳光标记蛋白 30 (SMP30) 表达的影响。

基本信息

批准号：
06833018
负责人：
FUJITA Toshiko
金额：
$ 1.34万
依托单位：
Tokyo Metropolitan Institute of Gerontology
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1994
资助国家：
日本
起止时间：
1994 至 1995
项目状态：
已结题

项目摘要

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.

我们报道了一种新型的肝蛋白，其量与雄激素无关降低。我们将该蛋白指定为衰老标记蛋白蛋白-30（SMP30）。我们具有孤立的大鼠和编码SMP30的Hunan cdna克隆。SMP30。SMP30是一种钙结合蛋白，它在congium结合蛋白中也起着各种调节的作用，该蛋白质的作用是各种元素。肝细胞。有人提出，随着衰老衰老的SMP30的减少可能会导致衰老肝脏的钙信号传导系统的老年变化。肝脏中的SMP30量相对较大（2％）（2％），推导的氨基酸序列和人类SMP30的氨基酸序列与SMP30相似的SMP30相似的同源性（89％类似）的同源性（同时）。这些结果支持SMP30在组织特定的肝脏和肾脏的特定生物学功能中的潜在关键作用。SMP30在肝细胞和肾脏近端肾小管上皮上皮中仅表达，这两者都表现出了smp smp smp smp smp smp smp smp smp smp smp smp smp smp smp smp smp smp smp smp smp。治疗两种不同类型刺激剂后的补偿性肝细胞增殖和直接增生。任何实验条件都涉及肝细胞增殖和肝细胞死亡的体内诱导。SMP30被增殖的刺激均与DNA归因于DNA的相互依赖。增殖性刺激后的肝细胞，但与DNA合成和有丝分裂无关。我们检查了苯巴比妥的效果，苯巴比妥的作用是非常强大的解毒系统酶的诱导剂。结果表明SMP30与药物代谢系统的相位I酶无关。