Brain-Derived Neurotrophic Factor Regulates Ishikawa Cell Proliferation through the TrkB-ERK1/2 Signaling Pathway.
Brain-Derived Neurotrophic Factor Regulates Ishikawa Cell Proliferation through the TrkB-ERK1/2 Signaling Pathway.
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脑源性神经营养因子通过 TrkB-ERK1/2 信号通路调节 Ishikawa 细胞增殖
DOI：
10.3390/biom10121645
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发表时间：
2020-12-08
期刊：
影响因子：
5.5
通讯作者：
Zhou X
中科院分区：
文献类型：
--
作者：
Cao M;Niu Q;Xiang X;Yuan C;Iqbal T;Huang Y;Tian M;Zhao Z;Li C;Zhou X
(1)背景：子宫内膜调节是维持正常子宫生理的必要条件，这是由多种生长因子驱动的。子宫内膜产生的生长因子被认为与雌二醇-17-雌二醇(β-17，E_2)诱导的子宫内膜细胞增殖有关。在本研究中，我们发现E2可以诱导Ishikawa细胞(子宫内膜细胞系的细胞)分泌脑源性神经营养因子(BDNF)。此外，利用Ishikawa细胞来探讨BDNF对子宫内膜细胞的调节作用，并阐明其可能的机制。(2)方法：用不同浓度的BDNF(100、200、300、400、500 ng/mL)处理Ishikawa细胞。通过定量逆转录聚合酶链式反应检测各种增殖相关基因的mRNA表达水平，并通过敲除BDNF或抑制BDNF与其受体TrkB的结合来检测各种增殖相关基因的表达。通过对TrkB-ERK1/2信号通路进行Western blotting检测各种增殖相关基因的表达水平。(3)外源性BDNF可促进Ishikawa细胞的生长，而BDNF被抑制或TrkB被抑制则抑制其生长。同时，BDNF提高了细胞活力，增加了细胞增殖相关基因的表达，包括细胞周期蛋白D1和细胞周期蛋白E2。更重要的是，BDNF诱导的Ishikawa细胞增殖涉及ERK1/2信号通路。(4)结论：外源性E_2刺激子宫BDNF的表达，并通过TrkB-ERK1/2信号通路促进Ishikawa细胞的增殖。
(1) Background: Endometrial regulation is a necessary condition for maintaining normal uterine physiology, which is driven by many growth factors. Growth factors produced in the endometrium are thought to be related to the proliferation of endometrial cells induced by estradiol-17β (E2). In this study, we found that E2 can induce the secretion of brain-derived neurotrophic factor (BDNF) in Ishikawa cells (the cells of an endometrial cell line). Furthermore, Ishikawa cells were used in exploring the regulatory role of BDNF in endometrial cells and to clarify the potential mechanism. (2) Methods: Ishikawa cells were treated with different concentrations of BDNF (100, 200, 300, 400, and 500 ng/mL). The mRNA expression levels of various proliferation-related genes were detected through quantitative reverse transcription polymerase chain reaction, and the expression of various proliferation-related genes was detected by knocking out BDNF or inhibiting the binding of BDNF to its receptor TrkB. The expression levels of various proliferation-related genes were detected by performing Western blotting on the TrkB-ERK1/2 signaling pathway. (3) Results: Exogenous BDNF promoted the growth of the Ishikawa cells, but the knocking down of BDNF or the inhibition of TrkB reduced their growth. Meanwhile, BDNF enhanced cell viability and increased the expression of proliferation-related genes, including cyclin D1 and cyclin E2. More importantly, the BDNF-induced proliferation of the Ishikawa cells involved the ERK1/2 signaling pathway. (4) Conclusions: The stimulating effect of exogenous E2 on the expression of BDNF in the uterus and the action of BDNF promoted the proliferation of the Ishikawa cells through the TrkB-ERK1/2 signal pathway.
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影响因子：
2.1
作者：
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通讯作者：
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影响因子：
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通讯作者：
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