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首页> 外文期刊>Life sciences >Shear stress enhances prostacyclin release from endocardial endothelial cells.
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Shear stress enhances prostacyclin release from endocardial endothelial cells.

机译：剪应力会增强前列环素从心内膜内皮细胞的释放。

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摘要

The effect of shear stress on the release of prostacyclin (PGI2) from cultured endocardial endothelial cells (EECs) was investigated. EECs were harvested from the right ventricle (RV) and the left ventricle (LV) of porcine heart. Confluent EECs were incubated under various degrees of shear stress (0.2, 1, 4 and 6 dyne/cm2) and PGI2 release from each cell was measured. PGI2 release from LV-EECs and RV-EECs was enhanced by the elevation of shear stress in a shear-dependent manner with a rapid increase at the onset of flow; however, there was no significant difference in PGI2 production between RV-EECs and LV-EECs. production of PGI2 was significantly inhibited from cells exposed to 8-(dimetilamino) octyl 3,4,5-trymethoxybenzoate hydrochloride (10 and 100 microM: an inhibitor of intracellular calcium mobilization) or cyclopiazonic acid (10 microM: an endoplasmic reticulum Ca2+-ATPase inhibitor). These results indicate that shear stress enhances PGI2 release from cultured EECs and that mechanotransduction of shear stress depends on calcium mobilization in EECs.
机译：研究了剪切应力对培养的心内膜内皮细胞（EEC）释放前列环素（PGI2）的影响。从猪心脏的右心室（RV）和左心室（LV）收获EEC。将融合的EEC在不同程度的剪切应力（0.2、1、4和6达因/厘米2）下孵育，并测量每个细胞释放的PGI2。 LV-EECs和RV-EECs中PGI2的释放通过以剪切依赖的方式增加剪切应力而增强，并在流动开始时迅速增加。但是，RV-EEC和LV-EEC之间的PGI2产量没有显着差异。暴露于8-（二甲氨基）辛基3,4,5-三甲氧基苯甲酸酯盐酸盐（10和100 microM：细胞内钙动员抑制剂）或环吡唑酸（10 microM：内质网Ca2 + -ATPase）的细胞显着抑制了PGI2的产生抑制剂）。这些结果表明剪切应力增强了培养的EEC中PGI2的释放，剪切应力的机械传导取决于EEC中钙的动员。

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