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首页> 外文期刊>British Journal of Haematology >The oestrogen receptor GPER is expressed in human haematopoietic stem cells but not in mature megakaryocytes.
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The oestrogen receptor GPER is expressed in human haematopoietic stem cells but not in mature megakaryocytes.

机译:雌激素受体GPER在人类造血干细胞中表达,但在成熟的巨核细胞中不表达。

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摘要

Megakaryocytes are bone-marrow precursor cells that differentiate to produce blood platelets via intermediate cytoplasmic extensions known as proplatelets (Patel et al, 2005). Recent advances in the understanding of megakaryocyte differentiation and platelet formation have been mostly obtained by biological studies of cultured cells. Although platelet formation from megakaryocytes has been actively studied, the molecular mechanisms of this process are still incompletely understood. Growing evidence has accrued that sex hormones may play a crucial role during megakaryopoiesis (Kostyak & Naik, 2007). Accordingly, it has been shown that high levels of oestrogens and conventional hormone replacement therapies increase the number of megakaryocytes in mice (Perry et al,2000) and in postmenopausal women (Bord et al, 2000). Nagata et al (2003) have also shown that oestradiol can be synthesised by murine megakaryocytes and that oestradiol positively affects proplatelet formation. In addition, Bord et al (2004) reported that oestrogens can promote megakaryocyte proliferation and maturation, thereby modulating the expression of the classical oestrogen receptors (ER)alpha and ERbeta. We have previously demonstrated that oestrogens can potentiate platelet aggregation through a rapid and reversible ERbeta-mediated signalling (Moro et al, 2005) and that membrane lipid rafts coordinate this pathway (Reineri et al, 2007).
机译:巨核细胞是骨髓前体细胞,它们通过称为前血小板的中间细胞质延伸分化而产生血小板(Patel等,2005)。对巨核细胞分化和血小板形成的理解的最新进展大部分是通过培养细胞的生物学研究获得的。尽管已经积极研究了从巨核细胞形成血小板的方法,但该过程的分子机制仍不完全清楚。越来越多的证据表明,性激素可能在巨核细胞生成过程中起着至关重要的作用(Kostyak&Naik,2007)。因此,已经表明,高水平的雌激素和常规的激素替代疗法增加了小鼠(Perry等,2000)和绝经后妇女(Bord等,2000)中巨核细胞的数量。 Nagata等人(2003年)也表明,雌二醇可以通过鼠巨核细胞合成,并且雌二醇积极影响血小板的形成。此外,Bord等人(2004年)报道,雌激素可促进巨核细胞增殖和成熟,从而调节经典雌激素受体(ER)α和ERbeta的表达。我们以前已经证明,雌激素可以通过快速和可逆的ERbeta介导的信号传导增强血小板聚集(Moro等,2005),并且膜脂质筏可以协调该途径(Reineri等,2007)。

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