Premium
Regulation of Postimplantation Mouse Embryonic Growth by Maternal Vasoactive Intestinal Peptide
Author(s) -
SPONG CATHERINE Y.,
LEE SUSAN J.,
McCUNE SUSAN K.,
GIBNEY GRETCHEN,
ABEBE DANIEL T.,
BRENNEMAN DOUGLAS E.,
HILL JOANNA M.
Publication year - 1999
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1999.tb07882.x
Subject(s) - vasoactive intestinal peptide , decidua , biology , trophoblast , embryonic stem cell , embryogenesis , medicine , endocrinology , embryo , messenger rna , microbiology and biotechnology , andrology , neuropeptide , placenta , fetus , receptor , pregnancy , gene , genetics
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 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.