Division of Nephrology, Department of Internal Medicine, Hannover Medical School, Germany.
J Cell Mol Med. 2010 Jul;14(7):1922-34. doi: 10.1111/j.1582-4934.2009.00799.x. Epub 2009 Jun 5.
Rapid apoptotic cell engulfment is crucial for prevention of inflammation and autoimmune diseases and is conducted by special immunocompetent cells like macrophages or immature dendritic cells. We recently demonstrated that endothelial cells (ECs) also participate in apoptotic cell clearance. However, in contrast to conventional phagocytes they respond with an inflammatory phenotype. To further confirm these pro-inflammatory responses human ECs were exposed to apoptotic murine ECs and changes in thrombospondin-1 (TSP-1) expression and in activation of intracellular signalling cascades were determined by real-time qPCR, immunoblotting and immunocytochemistry. Human primary macrophages or monocytic lymphoma cells (U937) were incubated with conditioned supernatant of human ECs exposed to apoptotic cells and changes in activation, migration and phagocytosis were monitored. Finally, plasma levels of TSP-1 in patients with anti-neutrophil cytoplasmic antibody(ANCA)-associated vasculitis (AAV) were determined by ELISA. We provided evidence that apoptotic cells induce enhanced expression of TSP-1 in human ECs and that this increase in TSP-1 is mediated by the mitogen-activated protein kinases (MAPK) ERK1 and 2 and their upstream regulators MEK and B-Raf. We also showed that plasma TSP-1 levels are increased in patients with AAV. Finally, we showed that conditioned supernatant of ECs exposed to apoptotic cells induces pro-inflammatory responses in monocytes or U937 cells and demonstrated that increased TSP-1 expression enhances migration and facilitates engulfment of apoptotic cells by monocyte-derived macrophages or U937 cells. These findings suggest that under pathological conditions with high numbers of uncleared dying cells in the circulation endothelial-derived elevated TSP-1 level may serve as an attraction signal for phagocytes promoting enhanced recognition and clearance of apoptotic cells.
快速的细胞凋亡吞噬对于预防炎症和自身免疫性疾病至关重要,由特殊的免疫细胞如巨噬细胞或未成熟树突状细胞执行。我们最近证明内皮细胞(ECs)也参与凋亡细胞的清除。然而,与传统的吞噬细胞不同,它们会表现出炎症表型。为了进一步证实这些促炎反应,我们将凋亡的鼠 EC 暴露于人 EC,并通过实时 qPCR、免疫印迹和免疫细胞化学测定血栓调节蛋白-1(TSP-1)表达和细胞内信号转导级联的激活变化。将人原代巨噬细胞或单核细胞淋巴瘤细胞(U937)与暴露于凋亡细胞的人 EC 条件培养基孵育,并监测激活、迁移和吞噬作用的变化。最后,通过 ELISA 测定抗中性粒细胞胞质抗体(ANCA)相关性血管炎(AAV)患者的血浆 TSP-1 水平。我们提供的证据表明,凋亡细胞诱导人 EC 中 TSP-1 的表达增强,而 TSP-1 的这种增加是由丝裂原活化蛋白激酶(MAPK)ERK1 和 2 及其上游调节因子 MEK 和 B-Raf 介导的。我们还表明,AAV 患者的血浆 TSP-1 水平升高。最后,我们表明,暴露于凋亡细胞的 EC 条件培养基诱导单核细胞或 U937 细胞的促炎反应,并证明增加的 TSP-1 表达增强迁移并促进单核细胞来源的巨噬细胞或 U937 细胞吞噬凋亡细胞。这些发现表明,在循环中未清除的死亡细胞数量较高的病理情况下,内皮细胞衍生的升高的 TSP-1 水平可能作为吞噬细胞的吸引信号,促进对凋亡细胞的增强识别和清除。