Buechler C, Ritter M, Quoc C D, Agildere A, Schmitz G
Klinikum der Universität Regensburg, Regensburg, D-93042, Germany.
Biochem Biophys Res Commun. 1999 Aug 19;262(1):251-4. doi: 10.1006/bbrc.1999.1193.
Human Cla-1 is the likely homologue of the murine scavenger receptor class B type I (SR-BI). SR-BI mediates selective transfer of cholesterol to high-density lipoprotein (HDL) and the efflux of endogenously synthesized and plasma membrane sterols to HDL. HDL protects against atherosclerosis but also reduces endotoxic activity by complexation and neutralization of LPS. We found that Cla-1 is upregulated during phagocytic as well as dendritic differentiation of monocytes, indicating a function of this receptor for cholesterol homeostasis in phagocytes and antigen-presenting cells. Cla-1 expression is suppressed by the proinflammatory stimuli lipopolysaccharide, interferon-gamma, and tumor necrosis factor alpha in monocytes and macrophages. Downregulation of Cla-1 mRNA by LPS is likely due to a modification and subsequent destabilization of the mRNA. We propose that suppression of Cla-1 expression may help to stabilize the lipoprotein status in the blood compartment important for host defense.
人Cla-1可能是小鼠I型B类清道夫受体（SR-BI）的同源物。SR-BI介导胆固醇向高密度脂蛋白（HDL）的选择性转移以及内源性合成的和质膜甾醇向HDL的流出。HDL可预防动脉粥样硬化，还可通过LPS的络合和中和作用降低内毒素活性。我们发现，Cla-1在单核细胞的吞噬以及树突状分化过程中上调，表明该受体在吞噬细胞和抗原呈递细胞的胆固醇稳态中发挥作用。Cla-1的表达在单核细胞和巨噬细胞中受到促炎刺激脂多糖、干扰素-γ和肿瘤坏死因子α的抑制。LPS对Cla-1 mRNA的下调可能是由于mRNA的修饰及随后的不稳定所致。我们提出，Cla-1表达的抑制可能有助于稳定血液中对宿主防御很重要的脂蛋白状态。
