Regulation of PGE(2) and PGI(2) release from human umbilical vein endothelial cells by actin cytoskeleton.
Regulation of PGE(2) and PGI(2) release from human umbilical vein endothelial cells by actin cytoskeleton.
复制标题
肌动蛋白细胞骨架对人脐静脉内皮细胞 PGE(2) 和 PGI(2) 释放的调节。
DOI：
10.1152/ajpcell.2001.281.3.c1038
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发表时间：
2001
期刊：
影响因子：
--
通讯作者：
Pavalko,FM
中科院分区：
文献类型：
--
作者：
Sawyer,SJ;Norvell,SM;Ponik,SM;Pavalko,FM
Disruption of microfilaments in human umbilical vein endothelial cells (HUVEC) with cytochalasin D (cytD) or latrunculin A (latA) resulted in a 3.3- to 5.7-fold increase in total synthesis of prostaglandin E2(PGE2) and a 3.4- to 6.5-fold increase in prostacyclin (PGI2) compared with control cells. Disruption of the microtubule network with nocodazole or colchicine increased synthesis of PGE21.7- to 1.9-fold and PGI21.9- to 2.0-fold compared with control cells. Interestingly, however, increased release of PGE2and PGI2from HUVEC into the media occurred only when microfilaments were disrupted. CytD treatment resulted in 6.7-fold more PGE2and 3.8-fold more PGI2released from HUVEC compared with control cells; latA treatment resulted in 17.7-fold more PGE2and 11.2-fold more PGI2released compared with control cells. Both increased synthesis and release of prostaglandins in response to all drug treatments were completely inhibited by NS-398, a specific inhibitor of cyclooxygenase-2 (COX-2). Disruption of either microfilaments using cytD or latA or of microtubules using nocodazole or colchicine resulted in a significant increase in COX-2 protein levels, suggesting that the increased synthesis of prostaglandins in response to drug treatments may result from increased activity of COX-2. These results, together with studies demonstrating a vasoprotective role for prostaglandins, suggest that the cytoskeleton plays an important role in maintenance of endothelial barrier function by regulating prostaglandin synthesis and release from HUVEC.
