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.
Gap junctions: maternal role in implantation
Gap junctions: maternal role in implantation. Development 1 August 2008; 135 (15): e1502. doi:
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As our publisher, The Company of Biologists, turns 100 years old, read about Development’s journey and highlights from some its first issues, and explore the history of each of our sister journals: Journal of Cell Science, Journal of Experimental Biology, Disease Models & Mechanisms and Biology Open.
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