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首页> 外文期刊>Journal of Cellular Physiology >Role of lipoxin A 4 in the cell-to-cell interaction between all-trans retinoic acid-treated acute promyelocytic leukemic cells and alveolar macrophages
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Role of lipoxin A 4 in the cell-to-cell interaction between all-trans retinoic acid-treated acute promyelocytic leukemic cells and alveolar macrophages

机译:在细胞间的角色lipoxin 4互动all-trans视黄酸洗急性早幼粒细胞白血病细胞和肺泡巨噬细胞

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Differentiation therapy with all-trans retinoic acid (ATRA) has been used successfully to treat acute promyelocytic leukemia (APL), but such treatment also causes differentiation syndrome (DS) by inducing APL cell infiltration into alveolar spaces. The mechanism underlying the clearance of infiltrated APL cells has not been investigated in detail. Lipoxin A 4 (LXA 4) is an important anti-inflammatory mediator during the resolution of inflammation. In this study, the role of LXA 4 in the cell-cell interaction between alveolar macrophages (AMφ{symbol}; NR8383 cells) and APL NB4 cells was investigated and found that conditioned medium (CM) harvested from ATRA-treated NR8383 (ATRA-NR8383) cells was able to induce the transmigration of ATRA-NB4 cells. However, the pro-migratory activity of CM was attenuated progressively when ATRA-NR8383 cells were co-cultured with increased cell dosages of apoptotic NB4 cells. A significantly higher amount of LXA 4 was released into the CM by ATRA-NR8383 cells when they were co-cultured with apoptotic ATRA-NB4 cells. Expression of a receptor for LXA 4 (ALX/FPR2) was enhanced in both ATRA-NB4 cells and ATRA-NR8383 cells. Exogenous LXA 4 treatment was able to inhibit the transmigration of ATRA-NB4 cells and induce the phagocytic clearance of apoptotic cells by ATRA-NR8383 cells. The anti-migratory activity of exogenous LXA 4 was attenuated by pre-treating ATRA-NB4 cells with an ALX/FPR2 inhibitor. We conclude that AMφ{symbol}-derived LXA 4 plays an important role in the interaction between AMφ{symbol} and APL cells and that this contributes to clearance of apoptotic APL cells.
机译:分化与all-trans维生素a治疗酸(ATRA)已被成功地用于治疗急性早幼粒细胞白血病(APL),但这样的治疗也会引起分化综合症(DS)诱导APL细胞浸润肺泡空间。清除渗透APL细胞没有详细调查。重要的抗炎介质在解决炎症。角色LXA 4的信息交互肺泡巨噬细胞(AMφ{象征};细胞)和APL NB4细胞研究发现条件培养液(CM)收获ATRA-treated NR8383 (ATRA-NR8383)细胞有能力诱导的轮回ATRA-NB4细胞。然而,CM的pro-migratory活动减毒逐步当ATRA-NR8383细胞被增加了培养细胞的剂量凋亡NB4细胞。数量的LXA 4被释放到厘米ATRA-NR8383细胞培养时凋亡ATRA-NB4细胞。LXA受体4 (ALX / FPR2)在增强ATRA-NB4细胞和ATRA-NR8383细胞。能够抑制外源性LXA 4治疗轮回ATRA-NB4细胞和诱导吞噬凋亡细胞的清除ATRA-NR8383细胞。外生LXA 4被预减毒ATRA-NB4细胞ALX / FPR2抑制剂。认为是φ}{象征派生LXA 4起重要的角色之间的交互是φ}{象征和APL细胞,这有助于清除凋亡APL细胞。

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