期刊论文详细信息
Endocrine Journal
Hyperglycemia perturbs biochemical networks in human trophoblast BeWo cells
Shinjiro Tachibana1  Hidekuni Inadera1  Mikiko Tatematsu1  Akiko Shimomura1  Ichiro Takasaki2 
[1] Department of Public Health, Faculty of Medicine, University of Toyama, Toyama, Japan;Division of Molecular Genetics Research, Life Science Research Center, University of Toyama, Toyama, Japan
关键词: Aromatase;    Diabetes;    Trophoblast;   
DOI  :  10.1507/endocrj.K10E-045
学科分类:内分泌与代谢学
来源: Japan Endocrine Society
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【 摘 要 】

References(38)Cited-By(3)Determining the effects of hyperglycemia on gene expression in placental trophoblast is important to gain a better understanding of how diabetes adversely affects pregnancy. In this study, we examined whether exposure to high glucose during forskolin-induced differentiation affects gene expression in differentiated trophoblasts. Human trophoblast BeWo cells were differentiated under low glucose (LG: 11 mM) or high glucose (HG: 25 mM) conditions. Gene expression was analyzed using a GeneChip system and the obtained data were analyzed using Ingenuity Pathways Analysis. In HG conditions, there were marked alterations in gene expression in differentiated BeWo cells compared with LG conditions. In particular, BeWo cells responded to HG with major changes in the expression levels of cell cycle- and metabolismrelated genes. We selected the aromatase gene for further investigation of the molecular mechanisms. Mannitol or 3-Omethylglucose did not mimic the expression changes caused by HG, indicating that the effect of glucose was not due to a difference in osmotic pressure, and that glucose metabolism plays an essential role in inducing the HG effects. Cotreatment with N-acetylcysteine reduced the effect of HG on aromatase gene expression, suggesting that hyperglycemia may perturb biochemical networks because of the elevation of oxidative stress. Overall, our results will aid further understanding of the effect of diabetes on the regulation of trophoblast differentiation and function.

【 授权许可】

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