Estrogen induced expression of the c-jun proto-oncogene in the immature and mature rat uterus

Webb, David; Moulton, Bruce C.; Khan, Sohaib A.

doi:10.1016/0006-291x(90)92381-9

Cited by 58 publications

(21 citation statements)

References 28 publications

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“…The initial phase of the mitogenic growth involves a series of early hypertrophic responses that appear 4 -6 h after hormone treatment and a series of late hyperplastic responses that develop 24 -30 h after hormone administration (29). The early responses induced by E 2 are characterized by altered expression of genes encoding for transcription factors (30), oncogenes (31)(32)(33), and growth factors and their receptors (34,35). Coupled with the changes in gene expression, dramatic changes in the structure and organization of the extracellular matrix have also been reported to occur in the early phases of the growth response (36).…”

Section: Discussionmentioning

confidence: 99%

In Vivo Regulation of Syndecan-3 Expression in the Rat Uterus by 17β-Estradiol

Russo¹,

Calabro²,

Filler³

et al. 2001

Journal of Biological Chemistry

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The immature rat uterus has been extensively used as an in vivo model system to study the molecular mechanisms of steroid hormone actions. In this study, we demonstrated the regulated expression of syndecan-3 in the rat uterus by the steroid hormone 17␤-estradiol. Administration of a single physiological dose of 17␤-estradiol (40 g/kg) to ovariectomized immature animals induced a rapid and transient increase in uterine syndecan-3 mRNA. Transcript levels reached a peak elevation of 3-fold above saline control tissues 4 h after hormone administration. Inhibition of message up-regulation by actinomycin D but not cycloheximide indicated a hormone response dependent on RNA transcription but not new protein synthesis. The estrogenic ligands estriol and tamoxifen were also effective at raising syndecan-3 mRNA levels; however, nonestrogenic ligands, including progesterone, 5␣-dihydrotestosterone, and dexamethasone, failed to stimulate a change in mRNA levels. Hormone-induced changes in mRNA led to transient changes in syndecan-3 protein content and significant alteration in the temporal and spatial expression in endometrial epithelial cells. Collectively, these data show that the steroid hormone 17␤-estradiol, regulates transcription of the syndecan-3 gene in the uterus via an estrogen receptor-dependent mechanism. This estrogen-regulated expression of syndecan-3 may play an important role in changes in tissue ultrastructure crucial for proper uterine growth.

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Section: Discussionmentioning

confidence: 99%

In Vivo Regulation of Syndecan-3 Expression in the Rat Uterus by 17β-Estradiol

Russo¹,

Calabro²,

Filler³

et al. 2001

Journal of Biological Chemistry

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“…During a normal estrous cycle, the expression of c-fos is regulated in association with cell proliferation, plasma estradiol (E2), and ER expression in the rat luminal epithelium (Mendoza-Rodrí guez et al 2003). It is well known that the uterine epithelial cells proliferate due to E2, and that the transcription of c-jun and c-fos genes is rapidly and dramatically induced in the uteri of ovariectomized immature and mature rats and mice treated with E2 or diethylstilbestrol (DES), a synthetic estrogen (Loose-Mitchell et al 1988, Weisz & Bresciani 1988, Webb et al 1990, Chiappetta et al 1992, Kamiya et al 1996. The estrogeninduced expressions of c-jun and c-fos are not prevented by protein synthesis inhibitors, suggesting a primary response to the ER complex.…”

Section: Introductionmentioning

confidence: 99%

Epithelial c-jun and c-fos are temporally and spatially regulated by estradiol during neonatal rat oviduct differentiation

Okada¹,

Ohta²,

Brody³

et al. 2004

Journal of Endocrinology

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Expression of transcription factors binding to the activating protein-1 (AP-1) site is induced by estrogens in association with epithelial proliferation in the uterus, but, in the oviduct, the relationship between cell proliferation and differentiation and AP-1 transcription factors is not well understood. In the developing rat oviduct, we found that proliferation and differentiation of epithelial cells were region-dependently regulated by 17 -estradiol (E2). To determine the role of AP-1 transcription factors in the development of rat oviduct, we performed immunohistochemistry for epithelial c-jun and c-fos proteins in E2-untreated and -treated newborn rats. E2 increased the expression of c-jun and c-fos during proliferation of undifferentiated epithelial cells, but diminished both proteins during accelerated differentiation of ciliated epithelial cells. A pure estrogen receptor (ER) antagonist, ICI 182,780, inhibited changes in their expression during both cell proliferation and differentiation. Importantly, no reduction of c-jun was noted in the epithelial cells of the foxj1-deficient oviduct, which lacks cilia development. This study shows that c-jun and c-fos are regulated during epithelial cell proliferation and differentiation in a regionspecific manner. This provides critical information for understanding the molecular and cellular mechanisms of the development of the neonatal oviduct.

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“…Interestingly, Tam oviduct (31). Differences in animal species status may explain why E2 increased the c-ju in rat uteri but decreased the levels in t E2-withdrawn chickens (51).…”

Section: Resultsmentioning

confidence: 99%

“…These gene the c-jun mRNA levels in the oviduct to Ta opposite responses generally observed for other known E2-60' 240' responsive genes (27)(28)(29)(30) 24). The c-jun protooncogene and the other jun family members have previously been reported to be rapidly regulated by several factors [e.g., by serum growth factors in BALB/c 3T3 mouse cells (26,38), by nerve growth factor in rat pheochromocytoma (PC-12) cells (39), and by transforming growth factor (3 in AkR-2B mouse embryo fibroblasts and other cells (40), by phorbol esters in mouse fibroblast cells (41), by the epidermal growth factor in rat fibroblasts (42), and finally by E2 in the rat uterus (51).…”

Section: Resultsmentioning

confidence: 99%

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Rapid induction of the c-jun protooncogene in the avian oviduct by the antiestrogen tamoxifen.

Lau

Subramaniam

Rasmussen

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

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This report describes a rapid regulation of the expression of the c-jun protooncogene by the antiestrogen tamoxifen (Tam). The c-jun protooncogene codes for an important component of the AP-1 transcription factor complex, which regulates the expression of many unlinked genes. Repeated experiments have shown that Tam rapidly increases the steady-state c-jun mRNA levels in the avian oviduct but decreases the levels in the liver. The Tam effects are time- and dose-dependent. These results are supported by other studies that have demonstrated that 17 beta-estradiol decreases steady-state levels of c-jun protooncogene mRNA in oviducts of animals fully withdrawn from estradiol. The effect of Tam in the avian oviduct is in contrast to the reported effects of Tam on the expression of practically all other genes in the avian oviduct and other animal tissues. Transcription analyses using nuclear runoff experiments with oviduct nuclei demonstrate a decrease in the c-jun gene transcription within minutes after Tam treatment with a return to 75% of control values by 4 hr. The fact that Tam transiently decreases the transcription of the c-jun gene but increases the steady-state c-jun mRNA levels suggests that Tam must alter both transcriptional and post-transcriptional events. The results support a role of the c-jun protooncogene as a regulatory gene in the cascade model for steroid action whereby steroids rapidly regulate the regulatory genes, which in turn regulate many other structural genes.

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Estrogen induced expression of the c-jun proto-oncogene in the immature and mature rat uterus

Cited by 58 publications

References 28 publications

In Vivo Regulation of Syndecan-3 Expression in the Rat Uterus by 17β-Estradiol

In Vivo Regulation of Syndecan-3 Expression in the Rat Uterus by 17β-Estradiol

Epithelial c-jun and c-fos are temporally and spatially regulated by estradiol during neonatal rat oviduct differentiation

Rapid induction of the c-jun protooncogene in the avian oviduct by the antiestrogen tamoxifen.

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