College of Pharmacy and Research Institute of Pharmaceutical Science, Sookmyung Women's University, Seoul, 140-742, Republic of Korea.
J Biomed Sci. 2010 Aug 24;17 Suppl 1(Suppl 1):S37. doi: 10.1186/1423-0127-17-S1-S37.
In the present study, we investigated the changes of uptake and efflux transport of taurine under various stress conditions using rat conditionally immortalized syncytiotrophoblast cell line (TR-TBT cells), as in vitro blood-placental barrier (BPB) model.
The transport of taurine in TR-TBT cells were characterized by cellular uptake study using radiolabeled taurine. The efflux of taurine was measured from the amount of radiolabeled taurine remaining in the cells after the uptake of radiolabeled taurine for 60 min.
Taurine uptake was significantly decreased by phosphorylation of protein kinase C (PKC) activator in TR-TBT cells. Also, calcium ion (Ca2+) was involved in taurine transport in TR-TBT cells. Taurine uptake was inhibited and efflux was enhanced under calcium free conditions in the cells. In addition, oxidative stress induced the change of taurine transport in TR-TBT cells, but the changes were different depending on the types of oxidative stress inducing agents. Tumor necrosis factor-alpha (TNF-alpha), lipopolysaccharide (LPS) and diethyl maleate (DEM) significantly increased taurine uptake, but H2O2 and nitric oxide (NO) donor decreased taurine uptake in the cells. Taurine efflux was down-regulated by TNF-alpha in TR-TBT cells.
Taurine transport in TR-TBT cells were regulated diversely at extracellular Ca2+ level, PKC activator and oxidative stress conditions. It suggested that variable stresses affected the taurine supplies from maternal blood to fetus and taurine level of fetus.
在本研究中,我们使用条件永生化的大鼠合体滋养层细胞系(TR-TBT 细胞)作为体外血胎盘屏障(BPB)模型,研究了在各种应激条件下牛磺酸摄取和外排转运的变化。
采用放射性标记牛磺酸的细胞摄取研究来表征 TR-TBT 细胞中牛磺酸的转运。在摄取放射性标记牛磺酸 60 分钟后,测量放射性标记牛磺酸在细胞中残留的量,以测量牛磺酸的外排。
PKC 激活剂磷酸化可显著降低 TR-TBT 细胞中的牛磺酸摄取。此外,钙离子(Ca2+)也参与了 TR-TBT 细胞中的牛磺酸转运。在细胞中无钙条件下,牛磺酸摄取受到抑制,外排增强。此外,氧化应激诱导了 TR-TBT 细胞中牛磺酸转运的变化,但变化因诱导氧化应激的试剂类型而异。肿瘤坏死因子-α(TNF-α)、脂多糖(LPS)和马来酸二乙酯(DEM)显著增加了牛磺酸摄取,但 H2O2 和一氧化氮(NO)供体减少了细胞中的牛磺酸摄取。TNF-α下调了 TR-TBT 细胞中的牛磺酸外排。
TR-TBT 细胞中的牛磺酸转运在外源性 Ca2+水平、PKC 激活剂和氧化应激条件下受到多样化调节。这表明不同的应激会影响母体血液向胎儿供应牛磺酸和胎儿牛磺酸水平。