Regulation of sterol synthesis in cultured cells by oxygenated derivatives of cholesterol
作者:
A. A. Kandutsch,
H. W. Chen,
期刊:
Journal of Cellular Physiology
(WILEY Available online 1975)
卷期:
Volume 85,
issue S1
页码: 415-424
ISSN:0021-9541
年代: 1975
DOI:10.1002/jcp.1040850408
出版商: Wiley Subscription Services, Inc., A Wiley Company
数据来源: WILEY
摘要:
AbstractSterol synthesis in liver in vivo is regulated at the site of the reaction catalyzed by 3‐hydroxy‐3‐methylglutaryl‐CoA reductase through a feedback system thought to involve either cholesterol or one or more of the products of its metabolism. Cholesterol feeding results in repression of the synthesis of the enzyme, but inactivation of the enzyme seems to precede repression of its synthesis. Sterol synthesis in cultured mouse liver cells and in L cell fibroblasts is not inhibited by purified exogenous cholesterol. However, derivatives of cholesterol produced by the introduction of a ketone or hydroxyl function in the 7, 20, 22 or 25 positions effectively inhibit sterol synthesis by specifically depressing the level of HMG CoA reductase activity. As a result of this specific effect prolonged incubation of an inhibitory sterol with growing L cells results in depletion of cellular sterol. Growth of the culture then ceases and the cells die unless an appropriate sterol or a sterol precursor is supplied in the medium. The inhibitory sterols, 25‐hydroxycholesterol and 7‐ketocholesterol appear to be taken up by L cells through processes that involve their specific interactions with saturable cellular receptors. The uptake of cholesterol by L cells appears to be by a different process — possibly through physi
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