Department of Internal Medicine I, University of Tuebingen, Tuebingen, Germany.
Autoimmunity. 2012 Dec;45(8):568-73. doi: 10.3109/08916934.2012.719947. Epub 2012 Sep 17.
Efficient engulfment of apoptotic cells is essential in multi-cellular organisms in order to prevent inflammatory responses. Apoptotic cells secure this process by releasing 'find-me' signals for the attraction of phagocytes. A major 'find-me' signal liberated from apoptotic cells is lysophosphatidylcholine (LPC). So far, however, the mechanisms underlying LPC release are poorly understood. In this study, we demonstrate that pharmacological inhibition and RNAi-mediated knock-down of the lipid transporter ABCA1 in apoptotic cells completely abolished phagocyte attraction. Moreover, ectopic expression of ABCA1 significantly enhanced monocyte migration to supernatants of apoptotic cells. Hence, ABCA1 represents a novel regulator of LPC release during apoptosis.
在多细胞生物中,有效地吞噬凋亡细胞对于防止炎症反应至关重要。凋亡细胞通过释放“寻我”信号来吸引吞噬细胞,从而确保了这个过程。凋亡细胞释放的一种主要“寻我”信号是溶血磷脂酰胆碱(LPC)。然而,到目前为止,LPC 释放的机制还知之甚少。在这项研究中,我们证明了在凋亡细胞中,通过药理学抑制和 RNAi 介导的 ABCA1 脂质转运蛋白敲低,完全消除了吞噬细胞的趋化作用。此外,ABCA1 的异位表达显著增强了单核细胞向凋亡细胞上清液的迁移。因此,ABCA1 是凋亡过程中 LPC 释放的一个新的调节因子。