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首页> 外文期刊>Cell and Tissue Research >Low density receptor-related protein 1 (LRP1) promotes anti-inflammatory phenotype in murine macrophages
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Low density receptor-related protein 1 (LRP1) promotes anti-inflammatory phenotype in murine macrophages

机译：低密度受体相关蛋白1（LRP1）促进小鼠巨噬细胞的抗炎表型

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摘要

We have previously reported that apolipoprotein E (apoE), a protein component of very-low-density lipoproteins (VLDL) and high-density lipoproteins and a potent plasma-borne atheroprotective factor, exerts anti-inflammatory activity in macrophages by switching the activation profile from M1 ("classic") to M2 ("alternative") in a process involving signaling via low-density lipoprotein receptor (LDLR) family members including the VLDL receptor (VLDLR) or apoE receptor-2 (apoER2). The present study was undertaken to investigate whether LDLR-related protein 1 (LRP-1), another member of the LDLR family and a ubiquitously expressed multifunctional cell surface receptor, modulates M1→M2 conversion in murine macrophages. We investigate bone marrow or peritoneal macrophages isolated from wild-type C57/Bl6 mice or mice with conditional inactivation of the LRP-1 gene in the myeloid lineage for the expression of polarization markers. Our results suggest that the deficiency of LRP-1 down-regulates M2 marker expression in macrophages, while enhancing the macrophage response to M1 stimuli. To our knowledge, this is the first demonstration that LRP-1 affects macrophage polarization and promotes the development of an anti-inflammatory M2 functional phenotype.
机译：先前我们曾报道过载脂蛋白E（apoE）是极低密度脂蛋白（VLDL）和高密度脂蛋白的一种蛋白质成分，是一种有效的血浆传播的抗动脉粥样硬化保护因子，可通过切换激活模式在巨噬细胞中发挥抗炎活性。从M1（“经典”）到M2（“替代”）的过程涉及通过低密度脂蛋白受体（LDLR）家族成员（包括VLDL受体（VLDLR）或apoE受体2（apoER2））进行信号传递。本研究旨在调查LDLR相关蛋白1（LRP-1），LDLR家族的另一个成员和普遍表达的多功能细胞表面受体是否调节鼠巨噬细胞中的M1→M2转化。我们调查从野生型C57 / Bl6小鼠或在髓系中LRP-1基因有条件失活的小鼠中分离出的骨髓或腹膜巨噬细胞，以表达极化标记。我们的结果表明，LRP-1的缺乏下调了巨噬细胞中M2标记的表达，同时增强了巨噬细胞对M1刺激的反应。据我们所知，这是LRP-1影响巨噬细胞极化并促进抗炎M2功能表型发展的第一个证明。

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