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首页> 外文期刊>Endothelium: Journal of endothelial cell research >Apoptosis in vascular endothelial cells caused by serum deprivation, oxidative stress and transforming growth factor-beta.
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Apoptosis in vascular endothelial cells caused by serum deprivation, oxidative stress and transforming growth factor-beta.

机译：血清剥夺，氧化应激和转化生长因子-β引起的血管内皮细胞凋亡。

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Vascular endothelial cell apoptosis has previously been shown to play a role in the pathogenesis of hypertension-induced vessel deletion and damage. In the present in vitro study we analyse several possible relevant causative factors of vascular endothelial cell apoptosis, namely, serum deprivation and nutrient depletion, oxidative stress in the forms of hypoxia, hyperoxia or free radical damage, and altered levels of transforming growth factor-beta1 (TGF-beta1) protein. An established cell line, bovine aortic endothelial cells (BAEC), was maintained in complete growth medium (RPMI-1640 plus 15% fetal calf serum and antibiotics, abbreviated as RPMI) in 25cm2 flasks or in 12-well plates on glass coverslips. Confluent but actively-growing cultures were treated with either hypoxia (PO2 of RPMI = 50mmHg), serum-free media (SFM), SFM plus hypoxia, hyperoxia (PO2 of RPMI = 450mmHg), hydrogen peroxide (H2O2, 1mM) in SFM, or TGF-beta1 protein (10ng/mL) in SFM. Appropriate control cultures were used. BAEC were collected 48h or 72h after all treatments except for TGF-beta1 and H2O2 treatments that were collected at 16-18h. Cell death was assessed using morphological characteristics or in situ end labeling (ISEL), cell proliferation assessed using proliferating cell nuclear antigen (PCNA), and TGF-beta1 expression assessed using transcript levels or immunohistochemistry. All treatments significantly increased levels of apoptosis over control cultures (P<0.05), and decreased levels of cell proliferation. Treatment with TGF-beta1 protein or SFM plus hypoxia induced greatest levels of apoptosis. TGF-beta1 protein and transcript levels were decreased in treated cultures, results suggesting that a paracrine source of TGF-beta1 protein would be needed as a cause of endothelial cell apoptosis in viva. Future therapies against inappropriate vessel deletion in disease states may use the known gene-driven nature of apoptosis to modify this sort of cell death in endothelial cells.
机译：血管内皮细胞凋亡先前已显示在高血压引起的血管缺失和损伤的发病机理中起作用。在目前的体外研究中，我们分析了血管内皮细胞凋亡的几种可能的相关原因，即血清剥夺和营养消耗，缺氧，高氧血症或自由基损伤形式的氧化应激以及转化生长因子β1水平的改变。 （TGF-beta1）蛋白。建立的细胞系牛主动脉内皮细胞（BAEC）被保存在25cm2烧瓶中或玻璃盖玻片的12孔板中的完全生长培养基（RPMI-1640加15％胎牛血清和抗生素，缩写为RPMI）中。融合但活跃生长的培养物在SFM中用低氧（RPMI的PO2 = 50mmHg），无血清培养基（SFM），SFM加缺氧，高氧（RPMI的PO2 = 450mmHg），过氧化氢（H2O2、1mM）处理，或SFM中的TGF-beta1蛋白（10ng / mL）。使用适当的对照培养物。在所有处理后48h或72h收集BAEC，但在16-18h收集TGF-beta1和H2O2处理除外。使用形态学特征或原位末端标记（ISEL）评估细胞死亡，使用增殖细胞核抗原（PCNA）评估细胞增殖，并使用转录水平或免疫组织化学评估TGF-beta1表达。与对照培养相比，所有处理均显着增加凋亡水平（P <0.05），并降低细胞增殖水平。用TGF-beta1蛋白或SFM加缺氧治疗可诱导最大程度的细胞凋亡。在处理过的培养物中，TGF-β1蛋白和转录物水平降低，结果表明，需要TGF-β1蛋白的旁分泌来源作为体内内皮细胞凋亡的原因。未来针对疾病状态中不适当的血管缺失的疗法可能使用已知的基因驱动的凋亡特性来修饰内皮细胞中的这种细胞死亡。

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