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首页> 外文期刊>Biochemistry >Apolipoprotein Al Deficiency Inhibits Serum Opacity Factor Activity against Plasma High Density Lipoprotein via a Stabilization Mechanism
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Apolipoprotein Al Deficiency Inhibits Serum Opacity Factor Activity against Plasma High Density Lipoprotein via a Stabilization Mechanism

机译：载脂蛋白Al缺乏通过稳定机制抑制血清不透明度因子活性对血浆高密度脂蛋白的影响

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摘要

The reaction of Streptococcal serum opacity factor (SOF) against plasma high-density lipoproteins (HDL) produces a large cholesteryl ester-rich microemulsion (CERM), a smaller neo HDL that is apolipoprotein (apo) AI-poor, and lipid-free apo AI. SOF is active versus both human and mouse plasma HDL. In vivo injection of SOF into mice reduces plasma cholesterol similar to 40% in 3 h while forming the same products observed in vitro, but at different ratios. Previous studies supported the hypothesis that labile apo AI is required for the SOF reaction vs HDL. Here we further tested that hypothesis by studies of SOF against HDL from apo AI-null mice. When injected into apo AI-null mice, SOF reduced plasma cholesterol similar to 35% in 3 h. The reaction of SOF vs apo AI-null HDL in vitro produced a CERM and neo HDL, but no lipid-free apo. Moreover, according to the rate of CERM formation, the extent and rate of the SOF reaction versus apo AI-null mouse HDL were less than that against wild-type (WT) mouse HDL. Chaotropic perturbation studies using guanidine hydrochloride showed that apo AI-null HDL was more stable than WT HDL. Human apo AI added to apo AI-null HDL was quantitatively incorporated, giving reconstituted HDL. Both SOF and guanidine hydrochloride displaced apo AI from the reconstituted HDL. These results support the conclusion that apo AI-null HDL is more stable than WT HDL because it lacks apo AI, a labile protein that is readily displaced by physicochemical and biochemical perturbations. Thus, apo AI-null HDL is less SOF-reactive than WT HDL. The properties of apo AI-null HDL can be partially restored to those of WT HDL by the spontaneous incorporation of human apo AI. It remains to be determined what other HDL functions are affected by apo AI deletion.
机译：链球菌血清不透明度因子（SOF）对血浆高密度脂蛋白（HDL）的反应产生大胆甾醇富含富含的微乳液（CERM），是一种较小的NEO HDL，其是载脂蛋白（APO）AI-PORS和脂质的APO艾。 SOF是活跃的与人和小鼠等离子体HDL。体内将SOF注入小鼠将血浆胆固醇与3小时相似的血浆胆固醇，同时形成在体外观察到的相同产品，但以不同的比例。以前的研究支持了SOF反应对HDL所需的假设。在这里，我们进一步通过SOF对来自APO Ai-unull小鼠的HDL的研究进行了测试。当注入Apo Ai-unly小鼠时，SOF减少血浆胆固醇，类似于3小时的35％。 SOF与体外的SOF与APO AI-NULL HDL的反应产生了CERM和NEO HDL，但不含脂质APO。此外，根据CERM形成的速率，SOF反应的程度和速率与APO AI-NULL小鼠HDL少于野生型（WT）小鼠HDL。使用盐酸胍的杂交扰动研究表明，APO Ai-Null HDL比WT HDL更稳定。已加入到APO AI-NULL HDL的人APO AI定量掺入，给予重构的HDL。 SOF和胍盐酸胍均由重构的HDL移位APO AI。这些结果支持AI-Null HDL比WT HDL更稳定的结论，因为它缺乏APO AI，一种通过物理化学和生物化学扰动容易移位的不稳定蛋白质。因此，APO AI-NULL HDL比WT HDL更少的SOF反应。通过人APO AI的自发掺入，可以将APO AI-NULL HDL的特性部分恢复到WT HDL的属性。它仍有待确定其他HDL函数受到apo ai删除的影响。

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  • 来源
    《Biochemistry》 |2015年第14期|共8页
  • 作者

    Rosales Corina; Patel Niket; Gillard Baiba K.; Yelamanchili Dedipya; Yang Yaliu; Courtney Harry S.; Santos Raul D.; Gotto Antonio M. Jr.; Pownall Henry J.;

  • 作者单位

    Houston Methodist Res Inst Dept Cardiol Lab Atherosclerosis &

    Lipoprot Res Houston TX 77030 USA;

    Houston Methodist Res Inst Dept Cardiol Lab Atherosclerosis &

    Lipoprot Res Houston TX 77030 USA;

    Houston Methodist Res Inst Dept Cardiol Lab Atherosclerosis &

    Lipoprot Res Houston TX 77030 USA;

    Houston Methodist Res Inst Dept Cardiol Lab Atherosclerosis &

    Lipoprot Res Houston TX 77030 USA;

    Houston Methodist Res Inst Dept Cardiol Lab Atherosclerosis &

    Lipoprot Res Houston TX 77030 USA;

    Univ Tennessee Hlth Sci Ctr Vet Affairs Med Ctr Memphis TN 38104 USA;

    Univ Sao Paulo Heart Inst INCOR BR-05409003 Sao Paulo Brazil;

    Houston Methodist Res Inst Dept Cardiol Lab Atherosclerosis &

    Lipoprot Res Houston TX 77030 USA;

    Houston Methodist Res Inst Dept Cardiol Lab Atherosclerosis &

    Lipoprot Res Houston TX 77030 USA;

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  • 正文语种 eng
  • 中图分类 生物化学;
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