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首页> 外文期刊>Journal of Cellular Physiology >Fibroblast growth factor 2 induces proliferation and distribution of G 2 2 /M phase of bovine endometrial cells involving activation of PI3K/AKT and MAPK cell signaling and prevention of effects of ER stress
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Fibroblast growth factor 2 induces proliferation and distribution of G 2 2 /M phase of bovine endometrial cells involving activation of PI3K/AKT and MAPK cell signaling and prevention of effects of ER stress

机译：纤维母细胞生长因子2诱导扩散和分布G 2 2 / M阶段的牛子宫内膜细胞的激活PI3K / AKT和细胞MAPK信号和预防ER应激的影响

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Fibroblast growth factor 2 (FGF2) is abundantly expressed in conceptuses and endometria during pregnancy in diverse animal models including domestic animals. However, its intracellular mechanism of action has not been reported for bovine endometrial cells. Therefore, the aim of this study was to identify functional roles of FGF2 in bovine endometrial (BEND) cell line which has served as a good model system for investigating regulation of signal transduction following treatment with interferon‐tau (IFNT) in vitro. Results of present study demonstrated that administration of FGF2 to BEND cells increased their proliferation and regulated the cell cycle through DNA replication by an increase of PCNA and Cyclin D1. FGF2 also increased phosphorylation of AKT, P70S6K, S6, ERK1/2, JNK, and P38 in BEND cells in a dose‐dependent manner, and expression of each of those transcription factors was inhibited by their respective pharmacological inhibitor including Wormannin, U0126, and SP600125. In addition, the increase in proliferation of BEND cells and activation of the protein kinases in response to FGF2 was suppressed by BGJ398, a FGFR inhibitor. Furthermore, proliferation of BEND cells was inhibited by tunicamycin, but treatment of BEND cells with FGF2 restored proliferation of BEND cells. Consistent with this result, the stimulated unfolded protein response (UPR) regulatory proteins induced by tunicamycin were down‐regulated by FGF2. Results of this study suggest that FGF2 promotes proliferation of BEND cells and likely enhances uterine capacity and maintenance of pregnancy by activating cell signaling via the PI3K and MAPK pathways and by restoring ER stress through the FGFR.
机译：纤维母细胞生长因子2 (FGF2)十分表示在孕体和子宫内膜在不同的动物模型包括怀孕国内的动物。的作用机制尚未报道牛子宫内膜细胞。本研究旨在识别功能的作用FGF2在牛子宫内膜(弯曲)细胞系作为一个好的模型系统吗调查调节信号转导用干扰素治疗后τ(IFNT)体外。管理FGF2弯曲细胞增加他们的扩散和调节细胞周期通过DNA复制PCNA的增加和细胞周期蛋白D1。一种蛋白激酶的磷酸化,P70S6K S6、ERK1/2物,和P38弯曲细胞一个剂量依赖的方式每个转录和表达被各自的抑制因素药理抑制剂包括Wormannin,U0126, SP600125。弯曲细胞和活化的扩散蛋白激酶在回应FGF2抑制由BGJ398 FGFR抑制剂。此外,弯曲细胞扩散由衣霉素抑制,但治疗弯曲与FGF2恢复细胞增殖的弯曲细胞。刺激的蛋白质反应(UPR)衣霉素引起的调控蛋白下来由FGF2监管。表明FGF2促进增殖的弯曲细胞和可能提高子宫和能力怀孕的维护通过激活细胞通过PI3K和MAPK信号通路通过FGFR恢复ER应激。

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