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人子宫内膜中缓激肽样免疫反应性的定位以及17β-雌二醇对缓激肽诱发的磷脂酶D活性的调节

Localisation of bradykinin-like immunoreactivity and modulation of bradykinin-evoked phospholipase D activity by 17 beta-oestradiol in human endometrium.

作者信息

Li X F, Ferriani R A, Michell R H, Ahmed A

机构信息

Reproductive Physiopathology Group, Medical School, University of Birmingham, Edgbaston, UK.

出版信息

Growth Factors. 1995;12(3):203-9. doi: 10.3109/08977199509036880.

Abstract

Bradykinin may act as a promoter of endometrial regeneration. Bradykinin-like immunoreactivity was detected immunocytochemically in the glandular epithelium and stroma of human endometrium. The staining was localized around the stroma and especially in the cells undergoing mitosis. Relatively weak staining was seen in the stromal cells of secretory endometrium, which was predominantly localised around the basal vacuoles of endometrial glands. During the late secretory phase, the intensity of staining was diminished throughout the endometrium: the glandular epithelium showed weak staining and stroma appeared negative. As phosphatidate, the product of phospholipase D pathway, may mediate cell proliferation, the effect of 17 beta-oestradiol on bradykinin-evoked phospholipase D activity assayed as accumulation of [3H]phosphatidylbutanol ([3H]PtdBut) was examined in [3H]myristic acid-labelled primary cultures of human endometrial stromal cells. Bradykinin induced a rapid accumulation of [3H]PtdBut in a time-dependent manner, indicating phospholipase D activation. Pretreatment of stromal cells with 17 beta-oestradiol enhanced the bradykinin-evoked phospholipase D activity. These results suggest that bradykinin-like immunoreactivity is strongly associated with proliferative stromal cells undergoing mitosis, a process that may be mediated by phospholipase D activation as the magnitude of this enzyme's activation in vitro appears to be regulated by 17 beta-oestradiol.

摘要

缓激肽可能作为子宫内膜再生的促进剂。通过免疫细胞化学方法在人子宫内膜的腺上皮和基质中检测到了缓激肽样免疫反应性。染色定位于基质周围,尤其是在进行有丝分裂的细胞中。在分泌期子宫内膜的基质细胞中可见相对较弱的染色,主要定位于子宫内膜腺的基底空泡周围。在分泌晚期,整个子宫内膜的染色强度减弱:腺上皮显示弱染色,基质呈阴性。由于磷脂酶D途径的产物磷脂酸可能介导细胞增殖,因此在[3H]肉豆蔻酸标记的人子宫内膜基质细胞原代培养物中检测了17β-雌二醇对缓激肽诱发的磷脂酶D活性(以[3H]磷脂酰丁醇([3H]PtdBut)的积累来测定)的影响。缓激肽以时间依赖性方式诱导[3H]PtdBut迅速积累,表明磷脂酶D被激活。用17β-雌二醇预处理基质细胞可增强缓激肽诱发的磷脂酶D活性。这些结果表明,缓激肽样免疫反应性与正在进行有丝分裂的增殖性基质细胞密切相关,这一过程可能由磷脂酶D激活介导,因为该酶在体外的激活程度似乎受17β-雌二醇调节。

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