Immunohistochemical studies on the expression and estrogen dependency of EGF and its receptor and C‐fos proto‐oncogene in the uterus and vagina of normal and neonatally estrogen‐treated mice

Falck, L; Forsberg, John‐Gunnar

doi:10.1002/(sici)1097-0185(199607)245:3<459::aid-ar2>3.3.co;2-2

Cited by 10 publications

(14 citation statements)

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“…The role of EGFR in the steroid-independent time period of neonatal uterine growth, however, is less well established. While the expression of both EGF and EGFR has been reported in the uterus of neonatal mice, no functional data exist (2,3). Our findings of decreased EGFR transcript and protein in the stroma of Hoxa11 mutants point, for the first time, to the potential importance of EGFR in the proper development of the uterus in neonatal mice.…”

Section: Discussionmentioning

confidence: 54%

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Hoxa11 Regulates Stromal Cell Death and Proliferation during Neonatal Uterine Development

Wong

Wintch

Capecchi

2004

Molecular Endocrinology

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Increasing evidence indicates that the Hoxa11 gene plays a critical role in the proper development of the uterus. In this report, we describe potential altered cellular processes in the developing uterus of Hoxa11 mutants. Histologic analysis demonstrates normal uterine morphology in Hoxa11 mutants as compared with controls at the newborn stage and d 7 after birth. Stromal tissue was moderately reduced in the Hoxa11 mutant uterus by d 14 after birth and was absent by d 21 after birth. There is decreased cellular proliferation in the Hoxa11 mutant uterus both at 7 and 14 d after birth. Terminal deoxyribonucleotide transferase-mediated deoxyuridine triphosphate nick-end labeling analysis demonstrates that apoptosis was markedly increased in the Hoxa11 mutant uterus at d 14 after birth. p27 is decreased in the Hoxa11 mutant as evidenced by real-time PCR. Epidermal growth factor receptor expression is dramatically decreased as evidenced by both real-time PCR and immunohistochemistry results. These findings suggest that Hoxa11 is required for proper cellular proliferation and apoptotic responses in the developing neonatal uterus and that the regulation of epidermal growth factor receptor is critical to these processes.

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Section: Discussionmentioning

confidence: 54%

“…Expression studies have revealed several factors present in the developing uterus including epidermal growth factor (EGF), EGF receptor (EGFR), keratinocyte growth factor (KGF), KGF receptor, and estrogen receptors (2)(3)(4)(5)(6). The importance of these genes in the proper development of the female reproductive tract, however, has not been established.…”

mentioning

confidence: 99%

Hoxa11 Regulates Stromal Cell Death and Proliferation during Neonatal Uterine Development

Wong

Wintch

Capecchi

2004

Molecular Endocrinology

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“…Nuclear staining might indicate the translocation of the transcription factors to its place of action. C-fos has been described in porcine and mouse endometrium (Dubois et al 1993;Falck and Forsberg 1996) and in preimplantation embryos of several species such as the pig, mouse and sheep (Müller et al 1982;Whyte and Stewart 1989;Pal et al 1993;Xavier et al 1997). In the sheep, some individual blastocysts of the same gestational stage exhibited jun and fos transcripts, while others did not (Wu 1996).…”

Section: Discussionmentioning

confidence: 99%

Expression of proto-oncogenes in bovine preimplantation blastocysts

Tetens¹,

Kliem²,

Tscheudschilsuren³

et al. 2000

Anatomy and Embryology

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Proto-oncogenes are involved in the regulation of gene expression, for example after ligand binding to growth factor receptors. Expression of the proto-oncogenes c-fos, c-jun, c-ha-ras and c-myc was studied in in vivo grown and in vitro cultured bovine preimplantation blastocysts employing RT-PCR, ribonuclease protection assay and immunohistochemistry. Thirteen- and 14- day-old preimplantation blastocysts, i.e. stages before and during trophoblast elongation, were used. In in vivo-grown blastocysts c-fos, c-jun and c-ha-ras transcripts as well as c-Fos, c-Jun and c-Myc proteins were detected in all stages studied. Cultured blastocysts were treated with 10 nM epidermal growth factor and 10 nM transforming growth factor-alpha simultaneously. Epidermal growth factor and transforming growth factor-alpha treatment induced c-fos mRNA and c-Myc protein expression. The induction of downstream targets of the epidermal growth factor receptor by epidermal growth factor and transforming growth factor-alpha indicates a functional epidermal growth factor signal transduction pathway in elongating bovine blastocysts.

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“…Thus, the irreversible proliferation of the vaginal epithelium in neonatally estrogenized mice is probably attributable to an estrogen-independent persistent activation downstream of estrogen signaling in the stromal cells. Indeed, a high level of expression of epidermal growth factor (EGF) is maintained in the vaginas of neonatally estrogenized mice even after ovariectomy (Falck and Forsberg 1996).…”

Section: Introductionmentioning

confidence: 99%

Prevention of neonatal estrogen imprinting by vitamin A as indicated by estrogen receptor expression in the mouse vagina

et al. 2001

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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.

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Immunohistochemical studies on the expression and estrogen dependency of EGF and its receptor and C‐fos proto‐oncogene in the uterus and vagina of normal and neonatally estrogen‐treated mice

Cited by 10 publications

References 0 publications

Hoxa11 Regulates Stromal Cell Death and Proliferation during Neonatal Uterine Development

Hoxa11 Regulates Stromal Cell Death and Proliferation during Neonatal Uterine Development

Expression of proto-oncogenes in bovine preimplantation blastocysts

Prevention of neonatal estrogen imprinting by vitamin A as indicated by estrogen receptor expression in the mouse vagina

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