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首页> 外文期刊>Journal of Cellular Physiology >Synergistic effect of high glucose and ANG II on proliferation of mouse embryonic stem cells: involvement of PKC and MAPKs as well as AT1 receptor.
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Synergistic effect of high glucose and ANG II on proliferation of mouse embryonic stem cells: involvement of PKC and MAPKs as well as AT1 receptor.

机译：协同效应的高葡萄糖和ANG II小鼠胚胎干细胞的增殖:PKC和MAPKs AT1受体。

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摘要

This study examined the synergistic effect of high glucose levels and ANG II on proliferation and its related signal pathways using mouse embryonic stem (ES) cells. The combined use of a high glucose concentration (25 mM) and ANG II increased the level of [3H]thymidine/BrdU incorporation, and the number of cells compared with either treatment alone. Each treatment with high glucose or ANG II increased the cell population in the S phase compared with control, and the combined treatment of a high glucose concentration and ANG II significantly increased the number of cells in the S phase according to FACS analysis. Moreover, the high glucose-induced increase in [3H]thymidine incorporation was blocked by inhibiting the ANG II type 1 (AT1) receptor. The combined high glucose and ANG II significantly increased the STAT3 phosphorylation compared with high glucose or ANG II alone. ANG II stimulated the influx of Ca2+ in 25 mM glucose compared with 5 mM glucose. High glucose levels increase the level of PKC alpha, epsilon, and zeta translocation from the cytosol to the membrane fraction. In an examination of other signal pathways, the combined treatment significantly increased the level of p44/42, p38 MAPKs phosphorylation compared with either treatment alone. Indeed, the combined treatment increased the mRNA expression level of the protooncogenes and cell cycle regulatory proteins. In conclusion, the combined treatment of a high glucose concentration and ANG II had a synergistic effect in stimulating mouse ES cell proliferation through the Ca2+/PKC, MAPKs, and the AT1 receptor.
机译：本研究调查了高的协同效应血糖水平和核扩散和ANGⅱ相关信号通路使用老鼠胚胎(ES)的干细胞。葡萄糖浓度(25毫米)和ANG II增加的程度[3 h]胸苷/ BrdU结合,细胞的数量比较与单独治疗。高葡萄糖或ANGⅱ细胞增加人口在S期与控制相比,联合治疗的高葡萄糖浓度和ANG II显著增加在S期细胞的数量根据流式细胞仪分析。增加[3 h]胸腺嘧啶核苷掺入被抑制ANGⅱ1型(AT1)受体。大大增加了STAT3磷酸化相比之下,高葡萄糖或独自ANGⅱ。二世在25毫米刺激Ca2 +的涌入葡萄糖相比之下,5毫米葡萄糖。增加PKC的水平α,ε,ζ易位从胞质膜分数。信号通路,联合治疗p44/42水平的显著提高,人们MAPKs磷酸化与之相比单独治疗。增加了mRNA的表达水平protooncogenes和细胞周期调控蛋白质。高葡萄糖浓度和ANGⅱ协同效应在刺激小鼠ES细胞扩散通过Ca2 + / PKC, MAPKs,AT1受体。

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