At the periphery of the human placenta, trophoblast attaches to the uterine wall. The tissue interface contains many anchoring sites, with cytotrophoblast columns that form bridges between the overlying extraembryonic (villous) mesenchyme and the maternal decidual stroma beneath. From the periphery of these columns, large numbers of trophoblast cells detach, migrate through the decidua and eventually colonize and transform maternal arteries. In this way the placenta increases and gives priority to the maternal blood supply to the conceptus. We have shown that when early villous tissue is explanted on a collagen gel in serum-free medium, anchoring-site morphogenesis occurs. Thus, in the presence of placental mesenchyme but in the absence of maternal cells, contact with a permissive extracellular matrix (ECM) is necessary and sufficient for cytotrophoblast column development. Proliferation of trophoblast occurs, followed by differentiation into a columnar cell phenotype in which cells remain attached to one another and to the ECM. At this stage, interaction between fibronectin and integrin α5β1 at the cell surface stabilizes the column and the cells remain as a contiguous multilayered sheet. However, the addition of serum-free conditioned medium from first-trimester placental fibroblasts stimulates cytotrophoblast to detach from the distal column and migrate in streams across the ECM. The removal of insulin-like growth factor I (IGF-I) from the fibroblast medium decreases streaming activity, whereas the addition of exogenous IGF-I (10 ng/ml) to serum-free medium produces a streaming phenotype. In contrast, transforming growth factor β1 (10 ng/ml) maintains the cells in a tight sheet. These results suggest the possibility of a paracrine interaction between villous mesenchyme and cytotrophoblast in anchoring sites to stimulate the infiltration of the maternal ECM by trophoblast. Such a mechanism would be self-limiting because the signal diminishes with distance from the placenta.
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Conference Article|
February 01 2000
Growth factor-extracellular matrix synergy in the control of trophoblast invasion
J. D. Aplin;
J. D. Aplin
1School of Medicine and School of Biological Sciences, University of Manchester, Research Floor, St Mary's Hospital, Manchester MI3 0JH, U.K.
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H. Lacey;
H. Lacey
1School of Medicine and School of Biological Sciences, University of Manchester, Research Floor, St Mary's Hospital, Manchester MI3 0JH, U.K.
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T. Haigh;
T. Haigh
1School of Medicine and School of Biological Sciences, University of Manchester, Research Floor, St Mary's Hospital, Manchester MI3 0JH, U.K.
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C. J. P. Jones;
C. J. P. Jones
1School of Medicine and School of Biological Sciences, University of Manchester, Research Floor, St Mary's Hospital, Manchester MI3 0JH, U.K.
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C.-P. Chen;
C.-P. Chen
1School of Medicine and School of Biological Sciences, University of Manchester, Research Floor, St Mary's Hospital, Manchester MI3 0JH, U.K.
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M. Westwood
M. Westwood
1School of Medicine and School of Biological Sciences, University of Manchester, Research Floor, St Mary's Hospital, Manchester MI3 0JH, U.K.
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Publisher: Portland Press Ltd
Received:
July 23 1999
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© 2000 Biochemical Society
2000
Biochem Soc Trans (2000) 28 (2): 199–202.
Article history
Received:
July 23 1999
Citation
J. D. Aplin, H. Lacey, T. Haigh, C. J. P. Jones, C.-P. Chen, M. Westwood; Growth factor-extracellular matrix synergy in the control of trophoblast invasion. Biochem Soc Trans 1 February 2000; 28 (2): 199–202. doi: https://doi.org/10.1042/bst0280199
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