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大鼠肝脏和类固醇生成组织中I型B类清道夫受体(一种高密度脂蛋白受体)的调节

Regulation of scavenger receptor, class B, type I, a high density lipoprotein receptor, in liver and steroidogenic tissues of the rat.

作者信息

Landschulz K T, Pathak R K, Rigotti A, Krieger M, Hobbs H H

机构信息

Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235, USA.

出版信息

J Clin Invest. 1996 Aug 15;98(4):984-95. doi: 10.1172/JCI118883.

Abstract

The scavenger receptor, class B, type I (SR-BI) binds HDL and mediates the selective transfer of cholesteryl esters from HDL to cultured cells. The tissue distribution of SR-BI in mice suggests that this receptor may deliver HDL-cholesterol to the liver and to nonplacental steroidogenic tissues. To examine the role of SR-BI in vivo, we determined its tissue and cell type-specific expression pattern and regulation in rats. High levels of immunodetectable SR-BI were present in the adrenal gland, ovary, and liver. In pregnant animals, the mammary gland also expressed high levels of the protein. SR-BI was localized by immunofluorescence to the surfaces of steroidogenic cells in the zona fasciculata and zona reticularis of the adrenal gland and to the corpus luteal cells of the ovary. High-dose estrogen treatment dramatically reduced SR-BI in the liver and increased SR-BI in the adrenal gland and corpus luteal cells of the ovary. These estrogen-induced increases in SR-BI in the adrenal gland and ovary were accompanied by enhanced in vivo uptake of fluorescent lipid from HDL. The administration of human chorionic gonadotropin induced a dramatic increase in SR-BI in the steroidogenic Leydig cells of the testes. These findings suggest that SR-BI mediates physiologically relevant uptake of cholesterol from HDL to nonplacental steroidogenic tissues in vivo.

摘要

清道夫受体B类I型(SR-BI)可结合高密度脂蛋白(HDL),并介导胆固醇酯从HDL向培养细胞的选择性转移。SR-BI在小鼠体内的组织分布表明,该受体可能将HDL胆固醇转运至肝脏和非胎盘类固醇生成组织。为了研究SR-BI在体内的作用,我们测定了其在大鼠体内的组织和细胞类型特异性表达模式及调控情况。在肾上腺、卵巢和肝脏中存在高水平可免疫检测到的SR-BI。在怀孕动物中,乳腺也表达高水平的该蛋白。通过免疫荧光法将SR-BI定位到肾上腺束状带和网状带的类固醇生成细胞表面以及卵巢的黄体细胞表面。高剂量雌激素处理显著降低了肝脏中的SR-BI,并增加了肾上腺和卵巢黄体细胞中的SR-BI。这些雌激素诱导的肾上腺和卵巢中SR-BI的增加伴随着体内从HDL摄取荧光脂质的增强。人绒毛膜促性腺激素的给药诱导睾丸类固醇生成间质细胞中SR-BI急剧增加。这些发现表明,SR-BI在体内介导了从HDL到非胎盘类固醇生成组织的生理相关胆固醇摄取。

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