Calcium regulates estrogen increase in permeability of cultured CaSki epithelium by eNOS-dependent mechanism.
Calcium regulates estrogen increase in permeability of cultured CaSki epithelium by eNOS-dependent mechanism.
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DOI：
10.1152/ajpcell.2000.279.5.c1495
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发表时间：
2000-11
期刊：
影响因子：
--
通讯作者：
G. Gorodeski
中科院分区：
文献类型：
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作者：
G. Gorodeski
雌激素增加跨CaSki培养物的基线跨上皮渗透性，并增强响应于高渗梯度的渗透性增加。在雌激素处理的细胞中，降低胞浆钙废除高渗诱导的增加渗透性和降低基线渗透性在更大程度上比雌激素剥夺细胞。稳态水平的胞浆钙在雌激素剥夺的细胞高于雌激素处理的细胞。细胞外钙离子的增加，增加胞浆钙在雌激素剥夺的细胞比在雌激素处理的细胞。然而，在雌激素处理的细胞中，增加胞浆钙离子与响应高渗梯度的渗透性比雌激素剥夺细胞更大的增加相关。降低胞浆钙可阻断雌激素诱导的一氧化氮（NO）释放和L-[（3）H]精氨酸体外转化为L-[（3）H]瓜氨酸的增加。用雌激素治疗可上调NO合酶亚型内皮型一氧化氮合酶（eNOS）的mRNA。这些结果表明，胞浆钙介导的反应，雌激素的渗透性增加和渗透性的增加，在响应高渗性涉及增加NO合成的钙依赖性eNOS的上调。
Estrogen increases baseline transepithelial permeability across CaSki cultures and augments the increase in permeability in response to hypertonic gradients. In estrogen-treated cells, lowering cytosolic calcium abrogated the hypertonicity-induced augmented increase in permeability and decreased baseline permeability to a greater degree than in estrogen-deprived cells. Steady-state levels of cytosolic calcium in estrogen-deprived cells were higher than in estrogen-treated cells. Increases in extracellular calcium increased cytosolic calcium more in estrogen-deprived cells than in estrogen-treated cells. However, in estrogen-treated cells, increasing cytosolic calcium was associated with greater increases in permeability in response to hypertonic gradients than in estrogen-deprived cells. Lowering cytosolic calcium blocked the estrogen-induced increase in nitric oxide (NO) release and in the in vitro conversion of L-[(3)H]arginine to L-[(3)H]citrulline. Treatment with estrogen upregulated mRNA of the NO synthase isoform endothelial nitric oxide synthase (eNOS). These results indicate that cytosolic calcium mediates the responses to estrogen and suggest that the estrogen increase in permeability and the augmented increase in permeability in response to hypertonicity involve an increase in NO synthesis by upregulation of the calcium-dependent eNOS.