title: Prevention of neonatal estrogen imprinting by vitamin A as indicated by estrogen receptor expression in the mouse vagina.
abstract: Treatment of female mice with estrogen during the neonatal period induces estrogen-independent persistent proliferation and cornification of the vaginal epithelium when the animals become adults. However, the occurrence of such irreversible vaginal changes is blocked by concurrent retinol acetate (RA) treatment. This study aimed to determine the expression pattern of estrogen receptor (ER) alpha and beta in the vaginas of ovariectomized 35-day-old mice treated neonatally with 17beta-estradiol (E(2)) and/or RA. The amounts of ERalpha and ERbeta mRNA molecules in the vaginal RNA samples were determined by competitive reverse transcription/polymerase chain reaction. The levels of both mRNAs were lower in ovariectomized mice that had been treated neonatally with E(2) but not in those treated with E(2) plus RA. Neonatal E(2) treatment caused a decrease in the percentage of ERalpha-immunoreactive cells in the vaginal stroma during adulthood, and concurrent RA treatment inhibited the decrease. The amount of each ER mRNA was also measured in the vaginas of mature mice treated with E(2) and RA; no inhibitory activity of RA was seen in the mature mice. Our studies indicate that, in mouse vagina, the irreversible effects of neonatal imprinting by estrogen might be prevented by the simultaneous administration of vitamin A through the inhibition of a decrease of the number of ER-expressing cells.
authors.affiliation: Department of Biological Sciences, Graduate School of Science, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. ss96341@mail.ecc.u-tokyo.ac.jp
authors.forename: F
authors.initials: F
authors.lastname: Masui
authors.forename: M
authors.initials: M
authors.lastname: Matsuda
authors.forename: Y
authors.initials: Y
authors.lastname: Akazome
authors.forename: T
authors.initials: T
authors.lastname: Imaoka
authors.forename: T
authors.initials: T
authors.lastname: Mori
mesh_terms: D000367:Age Factors; D000818:Animals; D000831:Animals, Newborn; D000906:Antibodies; D016588:Anticarcinogenic Agents / Q000494:pharmacology; D002455:Cell Division / Q000187:drug effects; D017931:DNA Primers; D004224:Diterpenes; D004347:Drug Interactions; D004847:Epithelial Cells / Q000737:chemistry / Q000166:cytology / Q000187:drug effects*; D004958:Estradiol / Q000494:pharmacology*; D047628:Estrogen Receptor alpha; D047629:Estrogen Receptor beta; D005260:Female; D051379:Mice; D008815:Mice, Inbred Strains; D010052:Ovariectomy; D011960:Receptors, Estrogen / Q000032:analysis / Q000235:genetics* / Q000276:immunology; D000084562:Retinyl Esters; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014621:Vagina / Q000737:chemistry / Q000166:cytology / Q000254:growth & development*; D014801:Vitamin A / Q000031:analogs & derivatives* / Q000494:pharmacology*
chemical_list: D000906:Antibodies; D016588:Anticarcinogenic Agents; D017931:DNA Primers; D004224:Diterpenes; D047628:Estrogen Receptor alpha; D047629:Estrogen Receptor beta; D011960:Receptors, Estrogen; D000084562:Retinyl Esters; D014801:Vitamin A; C009166:retinol acetate; D004958:Estradiol