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First published online July 11, 2008

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Gap junctions: maternal role in implantation

Over 50% of fertilised mammalian eggs fail to implant in the uterus. These failures are generally blamed on embryonic defects. Now, however, Laws and colleagues report that gap junction communication between uterine stromal cells drives the formation of new maternal blood vessels and is, therefore, crucial for embryo survival (see p. 2659). During early pregnancy, the steroid hormones oestrogen and progesterone control both the differentiation of uterine stromal cells into decidua (a secretory tissue) and uterine neovascularisation, two processes needed for successful embryo implantation. Oestrogen, the researchers report, stimulates the expression of the gap junction protein connexin 43 (Cx43) in mouse uterine stromal cells in vivo, and Cx43 expression, they show, is necessary for decidual differentiation, uterine neovascularisation and embryo survival. In vitro, human endometrial stromal cells do not differentiate into decidual cells or secrete the angiogenic factor VEGF when CX43 expression is ablated. Thus, the researchers conclude, Cx43-containing stromal gap junctions play a conserved and crucial role during implantation.

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Related articles in Development:

Gap junction communication between uterine stromal cells plays a critical role in pregnancy-associated neovascularization and embryo survival

Mary J. Laws, Robert N. Taylor, Neil Sidell, Francesco J. DeMayo, John P. Lydon, David E. Gutstein, Milan K. Bagchi, and Indrani C. Bagchi
Development 2008 135: 2659-2668. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in Development Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?