Regulation of human extravillous trophoblast function by membrane-bound peptidases
Regulation of human extravillous trophoblast function by membrane-bound peptidases
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DOI：
10.1016/j.bbapap.2005.04.007
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发表时间：
2005-08-01
影响因子：
3.2
通讯作者：
Maeda, M
中科院分区：
文献类型：
--
作者：
Fujiwara, H;Higuchi, T;Maeda, M
在人类胎盘形成过程中，绒毛外滋养层细胞侵入母体蜕膜组织，尤其是侵入母体螺旋动脉，被认为是随后正常胎儿发育的重要过程。然而，诱导EVT侵袭动脉和/或保护EVT免受进一步侵袭的确切调控机制还不是很清楚。最近，我们发现两种细胞表面肽酶DPPIV(DPPIV)和Cp-M(CP-M)在血管内皮细胞上有不同的表达。DPPIV的表达主要见于已停止侵袭的EVT。Cp-M表达于移行的动静脉血栓，包括母体动脉的血管内滋养细胞。这些肽酶的酶抑制作用影响了绒毛膜癌细胞系BeWo和JEG3的侵袭性。此外，趋化因子RANTES是DPPIV的底物之一，可增强从原代绒毛组织培养中分离的EVT的侵袭能力，其受体CCR1在向母体动脉迁移的EVT上特异性表达。此外，一种新的膜结合的细胞表面肽酶，命名为laeverin，被发现在几乎停止侵袭的血管内皮细胞上特异表达。这些发现表明，膜结合的多肽酶是调节人类早期胎盘EVT侵袭的重要因素。(C)2005 Elsevier B.V.保留所有权利。
During human placentation, the invasion of extravillous trophoblasts (EVTs) into maternal decidual tissues, especially toward maternal spiral arteries, is considered an essential process for Subsequent normal fetal development. However, the precise regulatory mechanisms to induce EVT invasion toward arteries and/or to protect EVTs from further invasion have not been well understood. Recently, we found that two cell surface peptidases, dipeptidyl peptidase IV (DPPIV) and carboxypeptidase-M (CP-M) are differentially expressed on EVTs. DPPIV expression was mainly observed on EVTs that had already ceased invasion. CP-M was detected on migrating EVTs including endovascular trophoblasts in the maternal arteries. The enzymatic inhibition of these peptidases affected the invasive property of choriocarcinoma-derived cell lines, BeWo and JEG3 cells. In addition, a chemokine, RANTES, that is one of the substrates for DPPIV, enhanced invasion of EVTs isolated from primary villous explant culture and its receptor, CCR1, was specifically expressed on migrating EVTs toward maternal arteries. Furthermore, a novel membrane-bound cell surface peptidase, named laeverin, was found to be specifically expressed on EVTs that had almost ceased invasion. These findings suggest that membrane-bound peptidases are important factors regulating EVT invasion during early placentation in humans. (c) 2005 Elsevier B.V. All rights reserved.