Abstract
Trophoblast invasion is crucial to placentation. The relationship between decidual glycodelin-A and trophoblast invasion is not known. Invasiveness of First trimester extravillous cytotrophoblast-1 (TEV-1) cell line, TEV-1, cells was determined by trans-well invasion assay. The gene expression, protein secretion and activities of the matrix metalloproteinase (MMP)-2 and -9, urokinase plasminogen activator (uPA), tissue inhibitor of metalloproteinase (TIMP)-1 and -2 and plasminogen activator inhibitor (PAI-1) of glycodelin-A-treated cells were measured by quantitative PCR, ELISA and gel zymography, respectively. Glycodelin-A bound to TEV-1 cells. At a concentration of 1 microg/ml, glycodelin-A, but not other glycodelin isoforms, suppressed the invasion of TEV-1 cells. The effect was glycosylation-dependent and was associated with reduction (P < 0.05) of MMP2, MMP9 and uPA activities in the conditioned medium from the treated culture. Glycodelin-A treatment suppressed the amount of MMP2 protein in the conditioned medium (P < 0.05) and MMP2 mRNA in the cells (P < 0.05), but did not affect that of MMP9. Glycodelin-A also significantly reduced the expression, secretion and activity of uPA (P < 0.05). The treatment did not affect the expression of TIMP-1, TIMP-2 or PAI-1, cell proliferation or survival of the cells. Glycodelin-A inhibits the invasion of extravillous cytotrophoblasts mainly by suppressing the activity of MMP2 and MMP9 in a glycosylation-dependent fashion.
Highlights
The invasion of the trophoblasts into the endometrium is crucial to placentation (Staun-Ram and Shalev, 2005; Lunghi et al, 2007)
Human trophoblast invasion is believed to be controlled by a balance between the actions of the stimulatory and inhibitory factors of both trophoblastic and uterine origins (Bischof et al, 2000)
Glycodelin-A is abundantly expressed in the decidua but not in the trophoblast (Seppala et al, 2002)
Summary
The invasion of the trophoblasts into the endometrium is crucial to placentation (Staun-Ram and Shalev, 2005; Lunghi et al, 2007). The key cells in placentation are the cytotrophoblasts (Staun-Ram and Shalev, 2005). The cytotrophoblasts differentiate into the villous cytotrophoblasts and the extravillous cytotrophoblasts (EVCTs). The villous cytotrophoblasts fuse to form the terminally differentiated multinucleated syncytiotrophoblasts responsible for fetomaternal exchange and production of hormones such as steroids and human chorionic gonadotrophin. The invasive EVCTs form migratory cell columns invading the endometrium (Lunghi et al, 2007). Some of the EVCTs invade the decidual stroma and the superficial myometrium to become the interstitial EVCTs, others invade the maternal spiral arteries to form the endovascular EVCTs
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