Ouellette M J, Hamel L, Tremblay N, Lamothe M, St-Jacques S
Unité de Recherche en Ontogénie et Reproduction, Universitaire de Québec, Pavillon CHUL, Ste-Foy, Canada.
J Reprod Fertil. 1999 Nov;117(2):229-39. doi: 10.1530/jrf.0.1170229.
During the oestrous cycle and early pregnancy, the uterus undergoes a variety of morphological and physiological modifications involving uterine cell proliferation and differentiation as well as extensive tissue remodelling. Transforming growth factor beta (TGF-beta) has powerful effects on these events and thus is thought to have a critical role in uterine physiology. Endoglin is a transmembrane glycoprotein that binds TGF-beta 1 and -beta 3 and interacts with TGF-beta signalling receptors to modulate many effects of this growth factor in different types of cell. Studies in mice revealed the highest concentrations of endoglin in the reproductive tract, notably on stromal cells of cyclic and pregnant uteri. The objective of the present study was to investigate the role of endoglin expressed on uterine stromal cells in binding TGF-beta and in the cellular responses induced by this growth factor. Highly purified populations of uterine stromal cells were isolated by cell affinity to the monoclonal antibody MJ7/18, which is specific to mouse endoglin. Affinity labelling of these cells with 125I-labelled TGF-beta followed by immunoprecipitation with endoglin-specific polyclonal 1256:4b antiserum indicated that endoglin expressed at the surface of uterine stromal cells binds TGF-beta 1 and interacts with TGF-beta signalling receptors. Treatment of uterine stromal cells with different concentrations of TGF-beta 1 induced a biphasic proliferative response and addition of MJ7/18 as well as neutralizing TGF-beta antibodies showed endoglin to be a modulator of TGF-beta-induced stromal cell proliferation. Given the importance of TGF-beta in the regulation of uterine physiology, these results indicate a role for endoglin during uterine tissue remodelling and decidualization.
在发情周期和妊娠早期，子宫会经历各种形态和生理变化，包括子宫细胞的增殖和分化以及广泛的组织重塑。转化生长因子β（TGF-β）对这些过程具有强大的作用，因此被认为在子宫生理学中起着关键作用。内皮糖蛋白是一种跨膜糖蛋白，它能结合TGF-β1和-β3，并与TGF-β信号受体相互作用，从而调节该生长因子在不同类型细胞中的多种效应。对小鼠的研究表明，生殖道中内皮糖蛋白的浓度最高，尤其是在周期性和妊娠子宫的基质细胞上。本研究的目的是探讨子宫基质细胞上表达的内皮糖蛋白在结合TGF-β以及该生长因子诱导的细胞反应中的作用。通过与小鼠内皮糖蛋白特异性的单克隆抗体MJ7/18进行细胞亲和，分离出高度纯化的子宫基质细胞群体。用125I标记的TGF-β对这些细胞进行亲和标记，然后用内皮糖蛋白特异性多克隆1256:4b抗血清进行免疫沉淀，结果表明子宫基质细胞表面表达的内皮糖蛋白能结合TGF-β1，并与TGF-β信号受体相互作用。用不同浓度的TGF-β1处理子宫基质细胞会诱导双相增殖反应，添加MJ7/18以及中和TGF-β抗体表明内皮糖蛋白是TGF-β诱导的基质细胞增殖的调节剂。鉴于TGF-β在调节子宫生理学中的重要性，这些结果表明内皮糖蛋白在子宫组织重塑和蜕膜化过程中发挥作用。
