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人子宫及配对的子宫平滑肌瘤中的鞘脂含量保持恒定。

Sphingolipid content in the human uterus and pair-matched uterine leiomyomas remains constant.

作者信息

Paweł Knapp, Chabowski Adrian, Górski Jan

机构信息

Department of Gynecology and Gynecological Oncology, Medical University of Bialystok, 24a Skłodowskiej Str., 15-269 Białystok, Poland.

出版信息

Lipids. 2013 Mar;48(3):245-50. doi: 10.1007/s11745-012-3746-2. Epub 2012 Dec 14.

DOI:10.1007/s11745-012-3746-2
PMID:23239114
Abstract

In the present work we sought to investigate the content of sphingolipids (sphingosine, sphinganine, sphingosine-1-phosphate and ceramide) in human fibroids and pair-matched healthy uterus tissue. We demonstrated that, in uterine leiomyomas, the contents of sphingosine, sphinganine, sphingosine-1-phosphate and ceramide remains quite constant. However, a trend towards elevation of ceramide and simultaneous reduction of sphingosine-1 phosphate levels was also noticed. Additionally, in uterine leiomyomas we found relevant activation of both PTEN and MAPK(ERK1/2) signaling pathways with only a minor change in AKT activity and relatively absent HIF-1α/AMPK activation. In conclusion, rather modest changes in sphingolipids are correlated with the activation of PTEN and MAPK(ERK1/2) signaling proteins in human uterine leiomyomas.

摘要

在本研究中,我们试图调查人类子宫肌瘤和配对的健康子宫组织中鞘脂(鞘氨醇、二氢鞘氨醇、鞘氨醇-1-磷酸和神经酰胺)的含量。我们证明,在子宫平滑肌瘤中,鞘氨醇、二氢鞘氨醇、鞘氨醇-1-磷酸和神经酰胺的含量保持相当稳定。然而,也注意到神经酰胺有升高趋势,同时鞘氨醇-1-磷酸水平降低。此外,在子宫平滑肌瘤中,我们发现PTEN和MAPK(ERK1/2)信号通路均有相关激活,AKT活性仅有微小变化,且相对缺乏HIF-1α/AMPK激活。总之,鞘脂的变化相当适度,与人类子宫平滑肌瘤中PTEN和MAPK(ERK1/2)信号蛋白的激活相关。

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本文引用的文献

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Horm Metab Res. 2012 Jun;44(6):436-41. doi: 10.1055/s-0031-1301301. Epub 2012 Feb 20.
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Ceramide synthase-dependent ceramide generation and programmed cell death: involvement of salvage pathway in regulating postmitochondrial events.依赖于神经酰胺合酶的神经酰胺生成和程序性细胞死亡:补救途径在调节线粒体后事件中的作用。
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Dysregulation of sphingolipid metabolism in cancer.癌症中鞘脂代谢的失调。
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HIF-mediated hypoxic response is missing in severely hypoxic uterine leiomyomas.严重缺氧的子宫肌瘤中缺乏 HIF 介导的缺氧反应。
Adv Exp Med Biol. 2010;662:399-405. doi: 10.1007/978-1-4419-1241-1_58.