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Hepatic expression of scavenger receptor class B type I (SR-BI) is a positive regulator of macrophage reverse cholesterol transport in vivo

机译:肝表达的清道夫受体B类I型(SR-BI)是一个积极的调节器。 巨噬细胞逆胆固醇 体内运输

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摘要

Hepatic expression of the scavenger receptor class B type I (SR-BI) promotes selective uptake of HDL cholesterol by the liver and is believed to play a role in the process of reverse cholesterol transport (RCT). We hypothesized that hepatic SR-BI expression is a regulator of the rate of integrated macrophage-to-feces RCT and used an in vivo model to test this hypothesis. Cholesterol-loaded and [3H]cholesterol-labeled J774 macrophages were injected intraperitoneally into mice, after which the appearance of the [3H]cholesterol in the plasma, liver, and feces over 48 hours was quantitated. Mice overexpressing SR-BI in the liver had significantly reduced [3H]cholesterol in the plasma but markedly increased [3H] tracer excretion in the feces over 48 hours. Conversely, mice deficient in SR-BI had significantly increased [3H]cholesterol in the plasma but markedly reduced [3H] tracer excretion in the feces over 48 hours. These studies demonstrate that hepatic SR-BI expression, despite its inverse effects on steady-state plasma HDL cholesterol concentrations, is an important positive regulator of the rate of macrophage RCT.
机译:肝脏表达的I类清道夫受体(SR-BI)促进肝脏对HDL胆固醇的选择性吸收,并被认为在胆固醇逆向转运(RCT)过程中起作用。我们假设肝脏SR-BI表达是巨噬细胞粪便RCT整合率的调节因子,并使用体内模型来检验该假设。腹膜内注射负载胆固醇和[3H]胆固醇标记的J774巨噬细胞,然后定量[48H]在血浆,肝脏和粪便中[3H]胆固醇的出现。在肝脏中过表达SR-BI的小鼠血浆中[3H]胆固醇含量显着降低,但在48小时内,粪便中[3H]示踪剂排泄量显着增加。相反,缺乏SR-BI的小鼠血浆中[3H]胆固醇显着增加,但在48小时内粪便中[3H]示踪剂排泄显着减少。这些研究表明,尽管肝SR-BI表达对稳态血浆HDL胆固醇浓度有反作用,但它仍是巨噬细胞RCT速率的重要正调节剂。

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