Effect of hypoxia on endothelin-1 production by pulmonary vascular endothelial cells.
Effect of hypoxia on endothelin-1 production by pulmonary vascular endothelial cells.
复制标题
缺氧对肺血管内皮细胞产生内皮素-1 的影响。
DOI：
10.1016/0167-4889(92)90033-8
复制
发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Guggino,WB
中科院分区：
文献类型：
--
作者：
Wiebke,JL;Montrose-Rafizadeh,C;Zeitlin,PL;Guggino,WB
内皮素-1(ET-1)是血管内皮细胞的多肽产物，对成纤维细胞和平滑肌细胞具有促有丝分裂作用。在本研究中，我们研究了低氧对牛肺血管内皮细胞产生ET-1的影响。分离牛肺动脉(BPAE)和微血管内皮细胞(BMVE)，在组织培养中生长，并鉴定其存在第VIII因子相关抗原和摄取低密度脂蛋白(LDL)。BPAE细胞产生ET-1的基线(用放射免疫测定法测定)随时间增加。在相同条件下，BMVE细胞产生ET-1的量是肺动脉内皮细胞的十分之一。在两种细胞中，低氧(0%O2)在48h显著降低ET-1的含量，在21%O2中恢复常氧48h，ET-1水平恢复到基线水平。Northern印迹分析显示，缺氧48h后，肺血管内皮细胞ET-1mRNA表达下降，提示肺血管内皮细胞对缺氧的反应是通过可逆地减少ET-1的产生来实现的，这种抑制作用可能是在转录水平上调节的。
Endothelin-1 (ET-1), a peptide product of endothelial cells, is mitogenic for fibroblasts and smooth muscle cells. In this study we examined the effect of hypoxia on ET-1 production by bovine pulmonary vascular endothelial cells. Bovine pulmonary artery (BPAE) and microvascular endothelial (BMVE) cells were isolated, grown in tissue culture, and characterized by the presence of Factor VIII related antigen and LDL uptake. Baseline production of ET-1 by BPAE cells (measured by8 radioimunoassay) increased over time. BMVE cells produced one tenth the amount of ET-1 as produced by the pulmonary artery endothelial cells under the same conditions. In both cell types, hypoxia (0% O2) significantly reduced the amount of ET-1 at 48 h. Restoration of normoxia in 21% O2for 48 h resulted in a return of ET-1 levels to baseline. Northern blot analysis showed decreased ET-1 mRNA in cells exposed to hypoxia for 48 h. These data demonstrate that pulmonary vascular endothelial cells respond to hypoxia by reversibly decreasing ET-1 production, and this attenuation is likely regulated at the level of transcription.