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首页> 外文期刊>Journal of Cellular Physiology >High glucose suppresses expression of equilibrative nucleoside transporter 1 (ENT1) in rat cardiac fibroblasts through a mechanism dependent on PKC-zeta and MAP kinases.
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High glucose suppresses expression of equilibrative nucleoside transporter 1 (ENT1) in rat cardiac fibroblasts through a mechanism dependent on PKC-zeta and MAP kinases.

机译：高葡萄糖抑制表达equilibrative核苷转运体1 (ENT1)大鼠心脏成纤维细胞通过一个机制激酶依赖PKC-zeta和地图。

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Recently it was demonstrated that the elevated concentration of glucose but not lack of insulin is responsible for suppression of equilibrative nucleoside transporter (ENT1) in diabetic rat cardiac fibroblasts (CFs). The present study was undertaken to determine the signaling pathway utilized by glucose to regulate the expression of ENT1 in the primary culture of rat CFs. Pretreatment of CFs with Go 6983, an isozyme non-selective PKC inhibitor, prevented the high glucose (25 mM) effect on ENT1 mRNA level and nitrobenzylthioinosine (NBTI)-sensitive adenosine uptake. Similar effect was observed with a cell-permeable PKC-zeta pseudosubstrate, whereas Go 6976 a selective inhibitor of Ca(2+)-dependent PKC-alpha and PKC-beta isozymes had little effect on high glucose-induced suppression of ENT1 mRNA level. Incubation of CFs with nitric oxide (NO) donors (SNAPE, SNP) or NO synthase inhibitors (L-NAME, L-NMMA) prior to exposition of CFs to high glucose did not change the glucose effect on ENT1 mRNA level. The high glucose-induced suppression of ENT1 expression was blocked by PD9859 (an inhibitor of MEK), whereas neither wortmannin (an inhibitor of PI3K) nor rapamycin (an inhibitor of mTOR) affected the glucose action on ENT1 transcript level. Highly effective in preventing the high glucose effect on ENT1 mRNA level were GW 5074 (an inhibitor of Raf kinase) and SB 203580 (selective p38 MAPK inhibitor). These findings indicate that high glucose suppresses the expression of ENT1 in CFs by NO independent manner involving the signaling through PKC-zeta, Raf-1, MEK, and p38 MAPK pathways.
机译：最近证明了高架葡萄糖但不缺乏胰岛素的浓度负责镇压equilibrative吗核苷转运体(ENT1)在糖尿病大鼠心脏成纤维细胞(CFs)。确定信号通路利用葡萄糖调节的表达ENT1鼠慢性疲劳综合症的主要文化。同工酶预处理的CFs 6983无选择性的PKC抑制剂,防止高葡萄糖(25毫米)ENT1 mRNA水平和影响吸收。cell-permeable PKC-zeta pseudosubstrate,而6976 Ca(2 +)的选择性抑制剂端依赖PKC-alpha和PKC-beta同功酶几乎没有影响高glucose-induced ENT1 mRNA的抑制的水平。捐助者(斯内普,SNP)或没有合酶抑制剂慢性疲劳综合症(L-NAME L-NMMA)博览会之前高葡萄糖没有改变葡萄糖效应ENT1 mRNA水平。被抑制的ENT1表达式PD9859 (MEK抑制剂),而不是渥曼青霉素(PI3K的抑制剂)和雷帕霉素(mTOR的抑制剂)影响葡萄糖ENT1行动记录水平。在预防ENT1高葡萄糖效应信使rna水平5074 GW (Raf的抑制剂203580(选择性p38 MAPK激酶)和某人抑制剂)。葡萄糖抑制ENT1在CFs的表达没有独立的方式涉及信号通过PKC-zeta、Raf-1 MEK和p38 MAPK通路。

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