Generation of neutrophil chemotactic activity by phorbol ester-stimulated calf pulmonary artery endothelial cells.

Generation of neutrophil chemotactic activity by phorbol ester-stimulated calf pulmonary artery endothelial cells.
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佛波酯刺激小牛肺动脉内皮细胞产生中性粒细胞趋化活性。

DOI:
10.1002/jlb.44.1.1
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发表时间:
1988
影响因子:
5.5
通讯作者:
Saba,TM
Saba,TM
中科院分区:
医学3区
文献类型:
--
作者:
Gudewicz,PW;Odekon,LE;DelVecchio,PJ;Saba,TM

文献摘要

被引文献

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用肉豆酸佛波酯(PMA)预处理单层小牛肺动脉内皮细胞1 ~ 4小时后,在无血清条件培养基中检测人多形核白细胞(PMNL)的趋化活性。在条件培养基中,PMA或亲脂活性较低的酚酯(4-β-酚-12,13-二丁酸P(Bu)2))预处理后,趋化活性呈剂量依赖性增加。通过棋盘分析证实了pma处理的内皮细胞条件培养基的趋化活性。pma预处理的内皮细胞在条件培养基中的趋化活性被环己亚胺、放线菌素D或脂氧合酶抑制剂二乙基卡马嗪预处理的内皮细胞完全抑制。此外,趋化活性是热稳定的,被胰蛋白酶抑制,并且在乙醚提取后存在于水相和脂相。数据表明,肺动脉内皮细胞暴露于活性磷酯释放有效的趋化因子(s) PMNL。这些发现表明,蛋白激酶C的激活剂在介导内皮细胞释放趋化因子中的作用,这可能在循环白细胞向血管损伤部位的定向迁移中很重要。
Chemotactic activity for human polymorphonuclear leukocytes (PMNL) was detected in serum-free conditioned media 1 to 4 hr after monolayers of calf pulmonary artery endothelial cells were pretreated with phorbol myristate acetate (PMA). Chemotactic activity was increased in conditioned media following pretreatment with either PMA or the less lipophilic active phorbol ester, 4-β-phorbol-12,13-dibutyrate (P(Bu)2) in a dose-dependent manner. Chemotactic activity of conditioned media from PMA-treated endothelial cells was confirmed by checkerboard analysis. The chemotactic activity in conditioned media from PMA-pretreated endothelial cells was completely inhibited by pretreating endothelial cells with either cycloheximide, actinomycin D, or the lipooxygenase inhibitor, diethylcarbamazine. Furthermore, the chemotactic activity was heat-stable, inhibited by trypsin treatment, and present in both aqueous and lipid phases after ether extraction. The data demonstrate that pulmonary artery endothelial cells exposed to active phorbol esters release potent chemotactic factor(s) for PMNL. These findings suggest a role for activators of protein kinase C in mediating endothelial cell release of chemotactic factor(s) that may be important in the directed migration of circulating leukocytes to sites of vascular injury.