Cultured endothelial cells increase their capacity to synthesize prostacyclin following the formation of a contact inhibited cell monolayer.
Cultured endothelial cells increase their capacity to synthesize prostacyclin following the formation of a contact inhibited cell monolayer.
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培养的内皮细胞在形成接触抑制细胞单层后增加了合成前列环素的能力。
DOI：
10.1002/jcp.1041140206
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发表时间：
1983
影响因子：
5.6
通讯作者：
Fuks,Z
中科院分区：
文献类型：
--
作者：
Eldor,A;Vlodavsky,I;Hy-Am,E;Atzmon,R;Weksler,BB;Raz,A;Fuks,Z
在活跃生长和接触抑制的牛主动脉内皮细胞培养物中研究了前列腺素（PG）、前列环素（PGI2）、PGE2和血栓烷A2（TXA2）的合成。通过暴露于外源性花生四烯酸或内过氧化物PGH2以及通过用蜂毒肽或离子载体A23187从细胞脂质中释放内源性花生四烯酸来刺激细胞合成洋地黄素。细胞合成PGI2和PGE2的能力增加，观察到作为培养时间的函数，无论刺激的类型。TXA2的产生仅在用离子载体A23187刺激细胞时才随时间增加。这种增加的PG合成能力是独立的细胞密度，因为它主要是在汇合，nondividing内皮细胞培养观察。PGH2是PGI2合成酶的直接刺激剂，在融合细胞中也观察到PGI2产量增加的事实，这意味着该过程与细胞内或培养基中的花生四烯酸浓度无关。这种增加的能力可能反映了与接触抑制内皮细胞单层形成相关的PG合成酶系统的活性增加。在培养的牛角膜内皮细胞生长期间，也观察到PGI2生产能力的类似时间依赖性增加。
The synthesis of the prostaglandins (PG), prostacyclin (PGI2), PGE2, and thromboxane A2(TXA2), has been investigated in actively growing and contact‐inhibited bovine aortic endothelial cell cultures. Cells were stimulated to synthesize prostaglandins by exposure to exogenous arachidonic acid or to the endoperoxide PGH2and by the liberation of endogenous arachidonic acid from cellular lipids with melittin or ionophore A23187. Increased capacity of the cells to synthesize PGI2and PGE2was observed as a function of time in culture, regardless of the type of stimulation. TXA2production increased with time only upon stimulation of the cells with ionophore A23187. This increased PG synthetic capacity was independent of cell density since it was mainly observed in confluent, nondividing endothelial cell cultures. The fact that increased PGI2production in confluent cells was also observed with PGH2, a direct stimulator of PGI2synthetase, implies that this process is independent of the arachidonate concentration within the cells or in the culture medium. This increased capacity is likely to reflect an increased activity of the PG synthetase system associated with the formation of a contact inhibited endothelial cell monolayer. A similar time‐dependent increase in the PGI2production capacity was also observed during growth of cultured bovine corneal endothelial cells.