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首页> 外文期刊>Cellular Physiology and Biochemistry >Linoleic Acid Induces Mouse Embryonic Stem Cell Proliferation Via Ca2+/PKC, PI3K/Akt, and MAPKs
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Linoleic Acid Induces Mouse Embryonic Stem Cell Proliferation Via Ca2+/PKC, PI3K/Akt, and MAPKs

机译：亚油酸通过Ca2 + / PKC，PI3K / Akt和MAPKs诱导小鼠胚胎干细胞增殖

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摘要

Aims: This study investigated the effect of linoleic acid (LA) on cell proliferation and the related signaling cascade in mouse embryonic stem (ES) cells. Materials & Methods: To examine effects of LA, mouse ES cells (ES-E14TG2a) were used. Moreover, DNA synthesis, glucose production, protein and mRNA expressions were measured. Results: LA increased DNA synthesis in a concentration-(>= 10(-9) M) and time(>= 24 h) dependent manner, as determined by [H-3] thymidine incorporation and increased cell number. LA increased intracellular Ca2+ levels via regulation of phospholipase C (PLC) and activated protein kinase C (PKC). LA activated phosphatidylinositol 3-kinase (PI3K)/Akt and p44/42 mitogen-activated protein kinases (MAPKs). U73122 (PLC inhibitor), staurosporine (PKC inhibitor), LY294002 (PI3K inhibitor), and Akt inhibitor blocked the phosphorylation of p44/42 MAPKs. In addition, LA stimulated gluconeogenesis through increase expression of glucose-6-phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (PEPCK). LA-induced increases in the cell cycle regulatory proteins, cyclin D1, cyclin E, cyclin-dependent kinase (CDK) 2, and CDK 4, were blocked by U73122, staurosporine, LY294002, Akt inhibitor, PD98059, and metformin (gluconeogenesis inhibitor). Conclusion: LA stimulated cell proliferation via Ca2+, PLC/PKC, PI3K/Akt, and p44/42 MAPKs signaling pathways in mouse ES cells.
机译：目的：本研究调查了亚油酸（LA）对小鼠胚胎干（ES）细胞增殖和相关信号传导级联的影响。材料与方法：为了检查LA的作用，使用了小鼠ES细胞（ES-E14TG2a）。此外，测定了DNA合成，葡萄糖产生，蛋白质和mRNA表达。结果：如[H-3]胸苷掺入和增加的细胞数所确定，LA以浓度（> = 10（-9）M）和时间（> = 24 h）依赖性的方式增加DNA合成。 LA通过调节磷脂酶C（PLC）和活化的蛋白激酶C（PKC）增加细胞内Ca2 +水平。 LA激活的磷脂酰肌醇3-激酶（PI3K）/ Akt和p44 / 42丝裂原激活的蛋白激酶（MAPK）。 U73122（PLC抑制剂），星形孢菌素（PKC抑制剂），LY294002（PI3K抑制剂）和Akt抑制剂可阻断p44 / 42 MAPK的磷酸化。另外，LA通过增加葡萄糖-6-磷酸酶（G6Pase）和磷酸烯醇丙酮酸羧化激酶（PEPCK）的表达来刺激糖异生。 LA诱导的细胞周期调节蛋白，细胞周期蛋白D1，细胞周期蛋白E，细胞周期蛋白依赖性激酶（CDK）2和CDK 4的增加被U73122，星形孢菌素，LY294002，Akt抑制剂，PD98059和二甲双胍（糖异生抑制剂）阻止。结论：LA通过Ca2 +，PLC / PKC，PI3K / Akt和p44 / 42 MAPKs信号通路刺激小鼠ES细胞的增殖。

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