Ca(2+)-dependent nitric oxide release in endothelial but not R3230Ac rat mammary adenocarcinoma cells.
Ca(2+)-dependent nitric oxide release in endothelial but not R3230Ac rat mammary adenocarcinoma cells.
复制标题
内皮细胞而非 R3230Ac 大鼠乳腺癌细胞中 Ca(2 ) 依赖性一氧化氮释放。
DOI：
10.1152/ajpcell.1996.271.1.c332
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Whorton,AR
中科院分区：
文献类型：
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作者：
Lindberg,RA;Dewhirst,MW;Buckley,BJ;Hughes,CS;Whorton,AR
我们已经表征了与实体瘤微血管系统相关的几种细胞类型释放一氧化氮（NO）的能力。响应于胞质Ca 2+浓度（[Ca 2 +]c）的增加。用Ca（2+）-ATP酶抑制剂毒胡萝卜素（TG）处理EA.hy926永生化的人脐静脉内皮细胞（EC）、大鼠成纤维细胞（RFL）和从R3230 Ac大鼠乳腺癌（MaC）分离的致瘤细胞。通过化学发光检测系统测量NO输出。基线NO输出仅可检测到EC。TG引起EC NO产量的显著增加，这种增加可以被NG-单甲基-L-精氨酸阻断，并被L-精氨酸恢复。TG不刺激RFL或MaC细胞释放NO，尽管在所有细胞中升高[Ca ~（2+）]c。NO合成酶（eNOS）的Ca（2+）依赖性亚型仅在EC中被免疫印迹检测到。这些数据表明，EC，而不是RFL或MaC，能够Ca（2+）依赖的NO.释放，并表明该肿瘤内的任何Ca（2+）依赖的NO.释放主要是内皮（而不是致瘤细胞）来源。
We have characterized the ability of several cell types associated with the microvasculature of solid tumors to release nitric oxide (NO.) in response to increases in cytosolic Ca2+ concentration ([Ca2+]c). EA.hy926 immortalized human umbilical vein endothelial cells (EC), rat fibroblasts (RFL), and tumorigenic cells isolated from R3230Ac rat mammary adenocarcinoma (MaC) were treated with thapsigargin (TG), an inhibitor of Ca(2+)-ATPase. NO. output was measured via a chemiluminescence detection system. Baseline NO. output was detectable only for EC. TG caused a significant increase in EC NO. output that could be blocked with NG-monomethyl-L-arginine and restored with L-arginine. TG did not stimulate NO. release from RFL or MaC cells, despite elevating [Ca2+]c in all cells. A Ca(2+)-dependent isoform of NO synthase (eNOS) was detected by immunoblot only in EC. These data indicate that EC, but not RFL or MaC, are capable of Ca(2+)-dependent NO. release and suggest that any Ca(2+)-dependent NO. release within this tumor is primarily of endothelial (and not tumorigenic cell) origin.