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首页> 外文期刊>Current opinion in lipidology >Atherosclerosis: cell biology and lipoproteins.
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Atherosclerosis: cell biology and lipoproteins.

机译：动脉粥样硬化：细胞生物学和脂蛋白。

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Chemokines are located on the surface of endothelial cells and within inflamed tissues, and are involved in the activation and extravasation of leukocytes. Recently, a number of well-performed studies have addressed the role of chemokines in leukocyte accumulation in atherosclerosis. Below, some of the data obtained from these studies are discussed. The role in atherosclerosis for CCR1 and CCR5, the receptors for the chemokine RANTES, were investigated in a set of papers. These two receptors are expressed mainly on mononuclear leukocytes and guide their trafficking to inflamed tissues. Previous data indicate that pharmacological disruption of RANTES signaling reduces atherosclerosis and the vulnerability of plaque in hypercholesterolemic mice; however, another study from 2005 showed that low-density lipo-protein receptor-deficient mice (LDLR~(-/-)) that received bone marrow from CCR1~(-/-) mice displayed an increase in atherosclerosis implicating that RANTES might exert its proatherogenic effects mainly through CCR5. The authors of the latter study have now performed bone marrow transplantation using CGRS~(-/-) mice as donors, and show that inflammatory activity as measured by lesion macrophage content and expression of matrix metalloproteinase-9 is attenuated when bone marrow-derived CCR5 is absent. There were, however, only limited effects on plaque size. These data stand in parallel to the findings by Zernecke et al., who demonstrated that deficiency in CCR5 protects against neointima formation after wire injury and this is followed by an increased expression of interleukin-10 in medial smooth muscle cells. Inhibition of interleukin-10 subsequently reversed the reduced neointimal formation in CCR5 mice implicating interleukin-10 in the effects of this chemokine. Data from an apolipoprotein E/CCR5 double-knockout model could also show lower numbers of lesion CD4~+ T cells together with reduced lesion size.
机译：趋化因子位于内皮细胞表面和发炎组织内，并参与白细胞的活化和外渗。近来，许多进行良好的研究已经解决了趋化因子在动脉粥样硬化中白细胞积累中的作用。下面，讨论了从这些研究中获得的一些数据。在一组论文中研究了CCR1和CCR5（趋化因子RANTES的受体）在动脉粥样硬化中的作用。这两个受体主要在单核白细胞上表达，并指导它们向发炎组织的运输。先前的数据表明，RANTES信号的药理学破坏可降低动脉粥样硬化和高胆固醇血症小鼠斑块的脆弱性。然而，2005年的另一项研究表明，从CCR1〜（-/-）小鼠接受骨髓治疗的低密度脂蛋白受体缺陷型小鼠（LDLR〜（-/-））显示出动脉粥样硬化的增加，提示RANTES可能发挥作用其促动脉粥样硬化作用主要通过CCR5。后者研究的作者现在已经使用CGRS〜（-/-）小鼠作为供体进行了骨髓移植，并显示了当源自骨髓的CCR5时，以病灶巨噬细胞含量和基质金属蛋白酶9的表达来衡量的炎症活性会减弱。缺席。但是，对斑块大小的影响有限。这些数据与Zernecke等人的发现平行，后者证明了CCR5的缺乏可防止金属丝损伤后新内膜的形成，随后白介素10在内侧平滑肌细胞中的表达增加。白细胞介素10的抑制随后逆转了CCR5小鼠中减少的新内膜形成，这牵涉白细胞介素10在这种趋化因子的作用。载脂蛋白E / CCR5双敲除模型的数据也可以显示出较少的病变CD4〜+ T细胞数量以及缩小的病变大小。

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