MEMBRANES AND PHOSPHOLIPIDS IN RENAL HYPERPLASIA
MEMBRANES AND PHOSPHOLIPIDS IN RENAL HYPERPLASIA
批准号:
3236011
负责人:
FREDERICK Gary TOBACK
金额:
$21.45万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
1986
资助国家:
美国
项目状态:
已结题
起止时间:
1986-04-01 至 1989-03-31
关键词:
acid phosphatase aminoacid autoradiography beta galactosidase beta glucuronidase bioenergetics cell differentiation cycloheximide dietary potassium electron microscopy electron transport histochemistry /cytochemistry hypokalemia immunochemistry kidney hyperplasia kidney metabolism lipid metabolism lysosomes membrane lipids membrane permeability membrane reconstitution /synthesis mitochondria nutrition related tag organelles oxidative phosphorylation phagocytosis phospholipids potassium deficiency radiotracer renal cortex renal medulla thin layer chromatography
中文摘要
这项研究的目的是阐明调节
膜形成、细胞器生物发生、细胞生长和能量代谢
在缺钾大鼠的肾脏中。
缺钾大鼠肾脏为器官功能的研究提供了一个特殊的模式系统
可以通过饮食变化来调节生长。 溶酶体的诱导
钾缺乏大鼠肾髓质的形成提供了一个独特的机会,
研究调节溶酶体生物合成和酶形成的因素。
线粒体氧化磷酸化对细胞凋亡的敏感性
膳食钾摄入允许研究这种离子在调节
细胞能量生产
我们计划使用缺钾大鼠的生长组织来表征钾在
作为磷脂和蛋白质前体摄取的调节剂,
磷脂生物合成的反应。 合成动力学和
特异性溶酶体酶的降解将由以下定义:
免疫沉淀分析和溶酶体形成的细胞位点将
在肾乳头的溶酶体生物发生和退化过程中进行研究,
缺钾和补钾大鼠。 K和其他阳离子在
线粒体能量的产生和糖酵解和
呼吸将在肾红细胞内条纹中的细胞中进行检查
髓质在钾耗竭时发生腺瘤样增生。
由于钾平衡的改变发生在许多疾病状态中,
生物化学和分子事件是这种干扰的后果,
对医学和无序生物学的基本重要性。
英文摘要
The objective of the proposed research is to elucidate mechanisms which regulate
membrane formation, organelle biogenesis, cellular growth and energy metabolism
in the kidneys of potassium (K)-depleted rats.
Kidneys of K-depleted rats offer an extraordinary mode system for study of organ
growth that can be modulated by dietary changes. The induction of lysosome
formation in the renal medulla of K-depleted rats provides a unique opportunity
to study the factors which regulate lysosome biogenesis and enzyme formation.
The sensitivity of mitochondrial oxidative phosphorylation to alterations in
dietary K intake permits study of the role of this ion in the regulation of
cellular energy production.
Using growing tissue from K-depleted rats we plan to characterize the role of K
as a modulator of phospholipid and protein precursor uptake and the enzymatic
reactions of phospholipid biosynthesis. The kinetics of synthesis and
degradation of a specific lysosomal enzyme will be defined by
immunoprecipitation analysis and the cellular locus of lysosome formation will
be studied during lysosome biogenesis and regression in the renal papilla of
K-depleted and K-repleted rats. The role of K and other cations in
mitochondrial energy production and in the integration of glycolysis and
respiration will be examined in cells in the inner stripe of the renal red
medulla which undergo adenomatous hyperplasia during K depletion.
Since alterations in K balance occur in many disease states, elucidation of the
biochemical and molecular events that are consequences of this disturbance is of
basic importance to medicine and disordered biology.
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