Pro-inflammatory cytokine-stimulated first trimester decidual cells enhance macrophage-induced apoptosis of extravillous trophoblasts.
Pro-inflammatory cytokine-stimulated first trimester decidual cells enhance macrophage-induced apoptosis of extravillous trophoblasts.
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DOI：
10.1016/j.placenta.2011.12.007
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发表时间：
2012-03
期刊：
影响因子：
3.8
通讯作者：
Huang, S. J.
中科院分区：
文献类型：
--
作者：
Wu, Z. -M.;Yang, H.;Li, M.;Yeh, C. -C.;Schatz, F.;Lockwood, C. J.;Di, W.;Huang, S. J.
当人胚泡衍生的绒毛外滋养层细胞（EVT）侵入早期蜕膜时，它们被定位成与免疫细胞和驻留的蜕膜细胞相互作用，并将螺旋动脉重塑成高容量血管，从而增加流向发育中的胎儿-胎盘单位的血流。浅的EVT侵犯会导致血管转化不完全，并减少子宫胎盘血流量，预示不良妊娠结局。蜕膜中过量的巨噬细胞通过分泌肿瘤坏死因子-α（TNF-α）诱导EVT凋亡。我们以前的观察，促炎细胞因子增强中性粒细胞和巨噬细胞激活剂粒细胞-巨噬细胞集落刺激因子（GM-CSF）的表达在早孕期蜕膜细胞现在扩展到包括：1）特定的巨噬细胞激活剂M-CSF; 2）巨噬细胞激活和随后的增强EVT细胞凋亡的GM-CSF和M-CSF。定量逆转录-聚合酶链反应和酶联免疫吸附试验评估了与白细胞介素-1 β（IL-1β）或TNF-α孵育的早孕蜕膜细胞中M-CSF的表达。将用来自蜕膜细胞培养物的条件培养基预孵育的外周单核细胞衍生的巨噬细胞与妊娠早期EVT细胞系HTR-8/SVneo细胞共培养。检测巨噬细胞活化，并通过DNA片段化、半胱天冬酶活化和细胞膜不对称性评价EVT凋亡。IL-1β或TNF-α可显著增强早孕蜕膜细胞M-CSF的表达。来自这些培养物的条件培养基激活巨噬细胞，巨噬细胞促进半胱天冬酶3/7依赖性EVT凋亡，抗GM-CSF或M-CSF的抗体阻断这种作用。促炎细胞因子增加早孕期蜕膜细胞M-CSF的合成。GM-CSF和M-CSF均激活巨噬细胞，巨噬细胞启动半胱天冬酶依赖性EVT凋亡。
As human blastocyst-derived extravillous trophoblasts (EVTs) invade the early decidua, they are positioned to interact with immune cells and resident decidual cells, and remodel spiral arteries into high capacity vessels that increase blood flow to the developing fetal-placental unit. Shallow EVT invasion elicits incomplete vascular transformation and reduces uteroplacental blood flow that presages adverse pregnancy outcomes. Excess macrophages in the decidua induce EVT apoptosis via tumor necrosis factor-alpha (TNF-α) secretion. Our previous observation that pro-inflammatory cytokines enhance neutrophil and macrophage activator granulocyte-macrophage colony-stimulating factor (GM-CSF) expression in first trimester decidual cells is now extended to include: 1) the specific macrophage activator M-CSF; 2) macrophage activation and subsequent enhancement of EVT apoptosis by both GM-CSF and M-CSF. Quantitative reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay assessed M-CSF expression in first trimester decidual cells incubated with interleukin-1 beta (IL-1β) or TNF-α. Peripheral monocyte-derived macrophages pre-incubated with conditioned media from decidual cell cultures were co-cultured with a first trimester EVT cell line, HTR-8/SVneo cells. Macrophage activation was examined and EVT apoptosis evaluated by DNA fragmentation, caspase activation and cell membrane asymmetry. IL-1β or TNF-α significantly enhanced M-CSF expression in first trimester decidual cells. The conditioned media from these cultures activates macrophages, which promote caspase 3/7-dependent EVT apoptosis with antibodies against GM-CSF or M-CSF blocking this effect. Pro-inflammatory cytokines increases synthesis of M-CSF in first trimester decidual cells. Both GM-CSF and M-CSF activate macrophages, which initiate caspase-dependent EVT apoptosis.
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3.8
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