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The proliferative effect of cortisol on bovine endometrial epithelial cells.
Reproductive Biology and Endocrinology ( IF 4.4 ) Pub Date : 2019-11-22 , DOI: 10.1186/s12958-019-0544-1
Junsheng Dong 1, 2 , Jun Li 1, 2 , Jianji Li 1, 2 , Luying Cui 1, 2 , Xia Meng 1, 2 , Yang Qu 1, 2 , Heng Wang 1, 2
Affiliation  

BACKGROUND Bovine endometrial epithelial cells (BEECs) undergo regular regeneration after calving. Elevated cortisol concentrations have been reported in postpartum cattle due to various stresses. However, the effects of the physiological level of cortisol on proliferation in BEECs have not been reported. The aim of this study was to investigate whether cortisol can influence the proliferation properties of BEECs and to clarify the possible underlying mechanism. METHODS BEECs were treated with different concentrations of cortisol (5, 15 and 30 ng/mL). The mRNA expression of various growth factors was detected by quantitative reverse transcription-polymerase chain reaction (qPCR), progression of the cell cycle in BEECs was measured using flow cytometric analysis, and the activation of the Wnt/β-catenin and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathways was detected with Western blot and immunofluorescence. RESULTS Cortisol treatment resulted in upregulated mRNA levels of vascular endothelial growth factor (VEGF) and connective tissue growth factor (CTGF); however, it had no influence on transforming growth factor-beta1 (TGF-β1). Cortisol (15 ng/mL) accelerated the cell cycle transition from the G0/G1 to the S phase. Cortisol upregulated the expression of β-catenin, c-Myc, and cyclinD1 and promoted the phosphorylation of PI3K and AKT. CONCLUSIONS These results demonstrated that cortisol may promote proliferation in BEECs by increasing the expression of some growth factors and activating the Wnt/β-catenin and PI3K/AKT signaling pathways.

中文翻译:

皮质醇对牛子宫内膜上皮细胞的增殖作用。

背景技术牛子宫内膜上皮细胞(BEEC)在产犊后会定期再生。据报道,由于各种压力,产后牛的皮质醇浓度升高。但是,尚未报道生理水平的皮质醇对BEECs中增殖的影响。这项研究的目的是调查皮质醇是否可以影响BEECs的增殖特性,并阐明可能的潜在机制。方法用不同浓度的皮质醇(5、15和30 ng / mL)处理BEEC。通过定量逆转录-聚合酶链反应(qPCR)检测各种生长因子的mRNA表达,使用流式细胞仪分析BEECs中细胞周期的进程,Western blot和免疫荧光检测Wnt /β-catenin和磷脂酰肌醇3-激酶(PI3K)/蛋白激酶B(AKT)信号通路的激活。结果皮质醇治疗导致血管内皮生长因子(VEGF)和结缔组织生长因子(CTGF)的mRNA水平上调。然而,它对转化生长因子β1(TGF-β1)没有影响。皮质醇(15 ng / mL)加速了细胞周期从G0 / G1到S期的转变。皮质醇上调β-catenin,c-Myc和cyclinD1的表达,并促进PI3K和AKT的磷酸化。结论这些结果表明,皮质醇可能通过增加某些生长因子的表达并激活Wnt /β-catenin和PI3K / AKT信号通路来促进BEEC的增殖。
更新日期:2020-04-22
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