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人生长激素与肝巨噬细胞结合的特性。

The characteristics of hGH binding to the liver macrophages.

作者信息

Kover K, Hung C H, Moore W V

出版信息

Horm Metab Res. 1986 Jan;18(1):26-30. doi: 10.1055/s-2007-1012217.

DOI:10.1055/s-2007-1012217
PMID:3005148
Abstract

Macrophages isolated from female rat liver as well as hepatocytes bind 125I-hGH. This study compares the effect of sex of the rat, hypophysectomy (hypox) and preincubation of the cells with oPrl on the binding of 125I-hGH to the cells. The percent of 125I-hGH to the hepatocytes was decreased in cells from hypox female and male rats, and hepatocytes preincubated with oPrl to 0.43, 0.21 and 0.39, respectively, of that observed in hepatocytes from normal female rats. In the hepatocytes from normal female, hypox female, and male rats, hGH was the most effective competitor for 125I-hGH binding with an ID50 of 0.73-0.99 nM. The concentration of oPrl, bGH and rGH that produced half-maximal inhibition (ID50) of 125I-hGH binding to hepatocytes from female rat liver was 6.3, 100, and 420 nM respectively. In hepatocytes from male and hypox female rats, and hepatocytes preincubated with oPrl, the ID50 for bGH and rGH varied from 2.1 to 15.9 nM. The percent of 125I-hGH bound by the macrophages from hypox female and male rats, and macrophages preincubated with oPrl was 0.06, 0.15 and 0.18, respectively, of that bound by macrophages from normal female rat liver. In contrast to hGH binding to the hepatocytes, the ID50 for hGH was 6 to 180-fold greater in macrophages from hypox female and male rats, and macrophages preincubated with oPrl compared to that observed in macrophages from normal female rats, Rat GH was the most effective competitor for 125I-hGH binding in the macrophages from the hypox female and male rat liver with ID50 of 5.5 and 85 respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

从雌性大鼠肝脏分离出的巨噬细胞以及肝细胞均可结合125I-hGH。本研究比较了大鼠性别、垂体切除(hypox)以及细胞与oPrl预孵育对125I-hGH与细胞结合的影响。来自hypox雌性和雄性大鼠的细胞以及与oPrl预孵育的肝细胞中,125I-hGH与肝细胞的结合百分比分别降至正常雌性大鼠肝细胞中观察值的0.43、0.21和0.39。在正常雌性、hypox雌性和雄性大鼠的肝细胞中,hGH是125I-hGH结合的最有效竞争者,ID50为0.73 - 0.99 nM。产生125I-hGH与雌性大鼠肝脏肝细胞结合半数最大抑制(ID50)的oPrl、bGH和rGH浓度分别为6.3、100和420 nM。在雄性和hypox雌性大鼠的肝细胞以及与oPrl预孵育的肝细胞中,bGH和rGH的ID50在2.1至15.9 nM之间变化。来自hypox雌性和雄性大鼠的巨噬细胞以及与oPrl预孵育的巨噬细胞结合的125I-hGH百分比分别为正常雌性大鼠肝脏巨噬细胞结合量的0.06、0.15和0.18。与hGH与肝细胞的结合情况相反,来自hypox雌性和雄性大鼠的巨噬细胞以及与oPrl预孵育的巨噬细胞中hGH的ID50比正常雌性大鼠巨噬细胞中观察到的ID50大6至180倍。大鼠生长激素(Rat GH)是hypox雌性和雄性大鼠肝脏巨噬细胞中125I-hGH结合的最有效竞争者,ID50分别为5.5和85。(摘要截取自250字)

相似文献

1
The characteristics of hGH binding to the liver macrophages.人生长激素与肝巨噬细胞结合的特性。
Horm Metab Res. 1986 Jan;18(1):26-30. doi: 10.1055/s-2007-1012217.
2
Comparison of hGH binding to isolated rat liver macrophages and hepatocytes.重组人生长激素与分离的大鼠肝脏巨噬细胞和肝细胞结合情况的比较。
Horm Metab Res. 1984 Apr;16(4):193-7. doi: 10.1055/s-2007-1014740.
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Binding of a variant of human growth hormone to liver plasma membranes.人生长激素变体与肝细胞膜的结合
Horm Metab Res. 1982 Mar;14(3):138-41. doi: 10.1055/s-2007-1018948.
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Interaction of human growth hormone with isolated rat liver cells.人生长激素与分离的大鼠肝细胞的相互作用。
Endocrinology. 1977 Jan;100(1):209-15. doi: 10.1210/endo-100-1-209.
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Growth hormone stimulation of glucose transport in isolated rat hepatocyte suspensions and primary cultures.生长激素对分离的大鼠肝细胞悬液和原代培养物中葡萄糖转运的刺激作用。
Endocrinology. 1981 Jan;108(1):239-46. doi: 10.1210/endo-108-1-239.
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Prolactin (PRL) receptor induction in cultured rat hepatocytes: dual regulation by PRL and growth hormone.培养的大鼠肝细胞中催乳素(PRL)受体的诱导:PRL和生长激素的双重调节
Endocrinology. 1988 Mar;122(3):1151-8. doi: 10.1210/endo-122-3-1151.
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Characterization and modulation of growth hormone and prolactin binding in mouse liver.小鼠肝脏中生长激素和催乳素结合的表征与调节
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Specific binding of human and bovine growth hormones to hypophysectomized rat hepatocytes.人和牛生长激素与垂体切除大鼠肝细胞的特异性结合。
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Specific binding of iodinated growth hormone to rat liver in vivo.碘化生长激素在体内与大鼠肝脏的特异性结合。
Endocrinology. 1978 Oct;103(4):1190-5. doi: 10.1210/endo-103-4-1190.
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Hepatic binding of human and bovine growth hormones and ovine prolactin in the dwarf "little" mouse.侏儒“小”鼠中人类和牛生长激素以及绵羊催乳素的肝脏结合情况
Endocrinology. 1983 Jun;112(6):2032-8. doi: 10.1210/endo-112-6-2032.

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