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低密度脂蛋白通过增加磷脂酰肌醇周转率和脂蛋白分解代谢导致全身细胞活化。

Low density lipoprotein causes general cellular activation with increased phosphatidylinositol turnover and lipoprotein catabolism.

作者信息

Block L H, Knorr M, Vogt E, Locher R, Vetter W, Groscurth P, Qiao B Y, Pometta D, James R, Regenass M

机构信息

Department of Medicine, University of Basel, Switzerland.

出版信息

Proc Natl Acad Sci U S A. 1988 Feb;85(3):885-9. doi: 10.1073/pnas.85.3.885.

Abstract

Low density lipoprotein (LDL), at concentrations high enough for receptor binding but not high enough to saturate the receptor, induces activation of phosphatidylinositol (PtdIns) turnover in a variety of cell types with various biological functions. Using both biochemical and electron microscopic studies, we have shown that blood platelets take up and degrade LDL in a manner reminiscent of phagocytic cell types. The activation of both PtdIns turnover and LDL metabolism is inhibited by high density lipoprotein. Thus, LDL at hormonal concentrations causes general cellular activation. Since all cell types studied responded to LDL with increased PtdIns turnover and uptake of LDL cholesterol, the PtdIns cycle may also be involved in the cellular regulation of LDL cholesterol metabolism.

摘要

低密度脂蛋白(LDL),其浓度高到足以与受体结合,但又不足以使受体饱和,可在多种具有不同生物学功能的细胞类型中诱导磷脂酰肌醇(PtdIns)代谢的激活。通过生化和电子显微镜研究,我们已经表明血小板摄取和降解LDL的方式类似于吞噬细胞类型。高密度脂蛋白可抑制PtdIns代谢的激活和LDL代谢。因此,激素浓度的LDL可引起一般细胞的激活。由于所有研究的细胞类型对LDL的反应都是PtdIns代谢增加和LDL胆固醇摄取增加,PtdIns循环可能也参与了LDL胆固醇代谢的细胞调节。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a5d/279661/e9d94cd468de/pnas00255-0255-a.jpg

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