Hypotonic shock stimulates ascorbate release from coronary artery endothelial cells by a Ca2+-independent pathway
Hypotonic shock stimulates ascorbate release from coronary artery endothelial cells by a Ca2+-independent pathway
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DOI：
10.1016/j.ejphar.2006.07.035
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发表时间：
2006-10-24
影响因子：
5
通讯作者：
Grover, Ashok K.
中科院分区：
文献类型：
--
作者：
Davis, Kim A.;Samson, Sue E.;Grover, Ashok K.
在内皮细胞中，在剪切应力和低渗休克期间，阴离子通道在渗透性肿胀时打开。因此，我们研究了低渗休克对猪冠状动脉内皮细胞释放抗氧化剂阴离子抗坏血酸的影响。低渗休克增强新鲜分离或培养的猪冠状动脉内皮细胞的抗坏血酸释放，随后培养的内皮细胞被使用。低渗休克引起的抗坏血酸释放的增加是迅速的，依赖于低渗休克的程度，而不是由于膜泄漏。用ATP刺激内皮细胞中的P2 Y（2）样受体通过Ca 2+介导的途径引起抗坏血酸释放。低渗休克诱导的释放不同于Ca 2+介导的Asc释放，因为：（a）低渗休克时释放的增加与ATP或A23187的增加是相加的（B）腺苷三磷酸双磷酸酶、苏拉明或去除细胞外Ca 2+均不影响低渗休克刺激的释放;（c）阴离子通道阻断剂不同程度地抑制两种途径的释放;低渗休克增加内皮细胞和培养的平滑肌细胞的抗坏血酸释放，而Ca ~（2+）介导的抗坏血酸释放仅发生在内皮细胞中。在细胞外抗坏血酸浓度为10（Na+-抗坏血酸同向转运体不饱和）和5000 μ M（Na+-抗坏血酸同向转运体饱和）时，检查内皮细胞的抗坏血酸积累。低渗休克和A23187在10 μ M抗坏血酸时减少抗坏血酸积累，但在5000 μ M时增加。两种处理的效果是加和的，并且用葡萄糖酸盐代替胞外氯也彼此不同。因此，内皮细胞的抗坏血酸释放可以通过两种不同的途径增强-低渗休克介导的和ATP/Ca 2+刺激的。(c)2006 Elsevier B. V.保留所有权利。
In endothelial cells, anion channels open upon osmotic swelling during shear stress and hypotonic shock. Therefore, we examined the effects of hypotonic shock on release of the antioxidant anion ascorbate from pig coronary artery endothelial cells. Hypotonic shock potentiated ascorbate release from freshly isolated or cultured pig coronary artery endothelial cells; subsequently cultured endothelial cells were used. The hypotonic shock-induced increase in Asc release was rapid, depended on the degree of hypotonic shock, and not due to membrane leakiness. Stimulating P2Y(2) like receptors in endothelial cells with ATP causes ascorbate release via a Ca2+-mediated pathway. Hypotonic shock-induced release differed from the Ca2+-mediated Asc release because: (a) the increase in release with hypotonic shock was additive to that with ATP or A23187 (Ca2+-ionophore), (b) apyrase, suramin or removing extracellular Ca2+ did not affect the hypotonic shock-stimulated release, (c) anion channel blockers inhibited the release by the two pathways differently, and (d) hypotonic shock increased the ascorbate release from endothelial cells and cultured smooth muscle cells whereas the Ca2+-mediated ascorbate release occurred only in endothelial cells. Accumulation of ascorbate by endothelial cells was examined at extracellular ascorbate concentrations of 10 (Na+-ascorbate symporter not saturated) and 5000 mu M (Na+-ascorbate symporter saturated). Hypotonic shock and A23187 decreased ascorbate accumulation at 10 mu M ascorbate but increased it at 5000 mu M. The effects of the two treatments were additive and also differed from each other with substitution of gluconate for extracellular chloride. Thus, ascorbate release from endothelial cells can be potentiated by two distinct pathways - hypotonic shock mediated and ATP/Ca2+ stimulated. (c) 2006 Elsevier B.V. All rights reserved.