Golpon Heiko A, Fadok Valerie A, Taraseviciene-Stewart Laima, Scerbavicius Robertas, Sauer Clemens, Welte Tobias, Henson Peter M, Voelkel Norbert F
Pulmonary Hypertension Center, University of Colorado, Health Sciences Center, Denver, Colorado, USA.
FASEB J. 2004 Nov;18(14):1716-8. doi: 10.1096/fj.04-1853fje. Epub 2004 Sep 2.
Removal of apoptotic cells by neighboring viable cells or professional phagocytes is essential for the maintenance of tissue homeostastis. Here we show that the phagocytosis of apoptotic Jurkat T cells by mouse epithelial cells (HC-11) and peritoneal macrophages leads to the secretion of growth and survival factors. We characterized VEGF as one of these factors which subsequently promote the proliferation of endothelial cells. Further we demonstrate that the phagocytosis of apoptotic bodies inhibits both spontanous and UV-irradiation-induced apoptosis in endothelial and epithelial cells. These effects were not observed when phagocytes had been exposed to viable or necrotic Jurkat T cells. We conclude that phagocytosis of apoptotic cells leads to secretion of growth and survival factors by phagocytes that represents a new form of life-promoting cell-cell interaction.
邻近的活细胞或专职吞噬细胞清除凋亡细胞对于维持组织稳态至关重要。在此我们表明,小鼠上皮细胞(HC-11)和腹腔巨噬细胞对凋亡Jurkat T细胞的吞噬作用会导致生长和存活因子的分泌。我们将血管内皮生长因子(VEGF)鉴定为这些因子之一,其随后可促进内皮细胞的增殖。此外,我们证明凋亡小体的吞噬作用可抑制内皮细胞和上皮细胞的自发性凋亡以及紫外线照射诱导的凋亡。当吞噬细胞接触活的或坏死的Jurkat T细胞时,未观察到这些效应。我们得出结论,凋亡细胞的吞噬作用会导致吞噬细胞分泌生长和存活因子,这代表了一种促进生命的新型细胞间相互作用形式。