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首页> 外文期刊>Journal of Lipid Research >Lipoprotein lipase mediates an increase in selective uptake of HDL-associated cholesteryl esters by cells in culture independent of scavenger receptor BI.
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Lipoprotein lipase mediates an increase in selective uptake of HDL-associated cholesteryl esters by cells in culture independent of scavenger receptor BI.

机译：脂蛋白脂肪酶介导培养物中与清道夫受体BI无关的细胞对HDL相关胆固醇酯选择性摄取的增加。

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摘要

Scavenger receptor class B type I (SR-BI) mediates the selective uptake of HDL cholesteryl esters (CEs) by the liver. LPL promotes this selective lipid uptake independent of lipolysis. In this study, the role of SR-BI in the mechanism of this LPL-mediated increase in selective CE uptake was explored. Baby hamster kidney (BHK) cells were transfected with the SR-BI cDNA, and significant SR-BI expression could be detected in immunoblots, whereas no SR-BI was visualized in control cells. Y1-BS1 murine adrenocortical cells were cultured without or with adrenocorticotropic hormone, and cells with no detectable or with SR-BI were obtained. These cells incubated without or with LPL in medium containing 125I/[3H]cholesteryl oleyl ether- labeled HDL3; tetrahydrolipstatin inhibited the catalytic activity of LPL. In BHK and in Y1-BS1 cells without or with SR-BI expression, apparent HDL3 selective CE uptake ([3H]CEt - 125I) was detectable. Cellular SR-BI expression promoted HDL3 selective CE uptake by approximately 250-1,900%. In BHK or Y1-BS1 cells, LPL mediated an increase in apparent selective CE uptake. Quantitatively, this stimulating LPL effect was very similar in control cells and in cells with SR-BI expression. The uptake of radiolabeled HDL3 was also investigated in human embryonal kidney 293 (HEK 293) cells that are an established SR-BI-deficient cell model. LPL stimulated [3H]cholesteryl oleyl ether uptake from labeled HDL3 by HEK 293 cells substantially, showing that LPL can induce selective CE uptake from HDL3 independent of SR-BI. To explore the role of cell surface proteoglycans on lipoprotein uptake, we induced proteoglycan deficiency by heparinase treatment. Proteoglycan deficiency decreased the LPL-mediated promotion of HDL3 selective CE uptake. In summary, evidence is presented that the stimulating effect of LPL on HDL3 selective CE uptake is independent of SR-BI and lipolysis. However, cell surface proteoglycans are required for the LPL action on selective CE uptake. It is suggested that pathways distinct from SR-BI mediate selective CE uptake from HDL.
机译：I类清道夫受体B（SR-BI）介导肝脏对HDL胆固醇酯（CEs）的选择性摄取。 LPL促进这种选择性脂质吸收，而与脂解作用无关。在这项研究中，探索了SR-BI在LPL介导的选择性CE摄取增加的机制中的作用。用SR-BI cDNA转染了小仓鼠肾（BHK）细胞，并且在免疫印迹中可以检测到明显的SR-BI表达，而在对照细胞中则看不到SR-BI。在没有或有促肾上腺皮质激素的情况下培养了Y1-BS1鼠肾上腺皮质细胞，得到了无可检测或SR-BI的细胞。这些细胞在没有或没有LPL的情况下在含有125I / [3H]胆固醇油基醚标记的HDL3的培养基中孵育;四氢他汀类药物抑制LPL的催化活性。在没有或没有SR-BI表达的BHK和Y1-BS1细胞中，可检测到明显的HDL3选择性CE摄取（[3H] CEt-125I）。细胞SR-BI表达促进HDL3选择性CE摄取约250-1,900％。在BHK或Y1-BS1细胞中，LPL介导表观选择性CE摄取增加。从数量上讲，这种刺激的LPL效应在对照细胞和具有SR-BI表达的细胞中非常相似。还研究了人类胚胎肾293（HEK 293）细胞中放射性标记HDL3的摄取，该细胞是已建立的SR-BI缺陷细胞模型。 LPL基本上由HEK 293细胞刺激了从标记的HDL3摄取[3H]胆甾醇基油基醚，表明LPL可以诱导HDL3选择性吸收CE，而与SR-BI无关。为了探索细胞表面蛋白聚糖对脂蛋白摄取的作用，我们通过肝素酶治疗诱导蛋白聚糖缺乏。蛋白多糖缺乏降低了LPL介导的对HDL3选择性CE摄取的促进。总之，有证据表明，LPL对HDL3选择性CE摄取的刺激作用与SR-BI和脂解作用无关。然而，LPL对选择性CE摄取的作用需要细胞表面蛋白聚糖。建议与SR-BI不同的途径介导HDL选择性摄取CE。

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