Study summary · research use only
Regulation of postimplantation mouse embryonic growth by maternal vasoactive intestinal peptide
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This mouse study examined vasoactive intestinal peptide (VIP) as a regulator of growth in the embryonic day (E) 9-11 mouse and sought the source of VIP at that stage. The abstract reports that VIP and its mRNA were detected in the decidua/trophoblast at E8 and declined until E10, after which VIP was not detectable, while VIP mRNA was not apparent in the embryo itself until E11-E12. At E9, some decidual cells showed VIP alongside lymphocyte markers (delta and CD3), and VIP binding sites were dense in the decidua/trophoblast at E6, decreasing until E10, with binding sites appearing in embryonic neuroepithelium by E9. The authors suggest that maternal decidual lymphocytes are the source of VIP regulating early postimplantation embryonic growth.
Abstract
Vasoactive intestinal peptide (VIP) is an identified regulator of growth in the embryonic day (E) 9-11 mouse. Mouse embryonic and extra-embryonic tissues were studied to identify the source of VIP at this critical time. VIP and mRNA was detected in the decidua/trophoblast at E8 and declined until E10, after which it was not detectable. VIP mRNA was not apparent in the embryo until E11-E12. At E9, cells in decidua had VIP as well as lymphocyte marker (delta and CD3) immunoreactivity. VIP binding sites were dense in the decidua/trophoblast at E6, which gradually decreased until E10. VIP binding sites were detected in embryonic neuroepithelium by E9. The transient presence of VIP binding sites and mRNA in the decidua/trophoblast correlate with the identified period of VIP growth regulation, when VIP mRNA is absent in the embryo. Therefore, these findings suggest that maternal decidual lymphocytes are the source of VIP that regulate early postimplantation embryonic growth.
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