Ontogeny of Estrogen Receptor Messenger Ribonucleic Acid Expression in the Postnatal Rat Uterus1

Fishman, Renata B.; Branham, William S.; Streck, Randal D.; Sheehan, Daniel M.

doi:10.1095/biolreprod55.6.1221

Cited by 23 publications

(20 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…After PND14, ER expression and PCNA positive cells were concurrently increased in the invaginated-luminal and glandular epithelium. In the OP-treated group, however, gland formation was delayed and inhibited as reported previously by us (22) and other investigators (6)(7)(8)26), although ER expression and PCNA positive In contrast, ER expression in stromal cells of the control group was observed at PND6, similar to many other reports (13,14,16,17,37), although no induction of PCNA positive cells was detected. OP treatment suppressed ER expression without PCNA alteration, in line with data for mice neonatally exposed to DES (40).…”

Section: Er (supporting

confidence: 88%

“…Sato et al (32) also reported early ER expression in the luminal epithelium of uteri induced by neonatal exposure to estrogens/anti-estrogens in mice, whereas other investigators indicated that cytosolic estrogen receptors were decreased in mice neonatally exposed to DES (6). In other studies ER expression in the uterine epithelium of control rats began to appear at various days from PND7 to PND15 (6,14), but was evident at PND14 in our study, suggesting a dependence on the strain difference as reported in mice (3), or the sensitivity of the detection method between immunohistochemical and radioimmunoassay techniques (14).…”

Section: Er (mentioning

confidence: 93%

See 1 more Smart Citation

Neonatal Exposure to p-tert-octylphenol Causes Abnormal Expression of Estrogen Receptor α and Subsequent Alteration of Cell Proliferating Activity in the Developing Donryu Rat Uterus

et al. 2002

View full text Add to dashboard Cite

In the present study, we investigated immunohistochemicall y the time-course alterations in estrogen receptor a (ER) expression and cell proliferating activity in the developing uteri of Donryu rats exposed neonatally to a high dose p-tert-octylpheno l (OP), an endocrine disrupting chemical (EDC). OP-treatment (sc injections of 100 mg/kg, every other day from postnatal days 1 to 15) induced an early and enhanced ER expression in the luminal epithelium compared with age-matched controls from postnatal day (PND) 10, and increased proliferating cell nuclear antigen (PCNA) positive cells up to PND21. At PND28, ER expression in the luminal epithelium of the OP-treated group was decreased, in association with decline in the luminal epithelial areas. PND14, the second week of life, is coincident with the normal time for differentiation when the luminal epithelium invaginates into the stroma to form uterine glands. OP-treatment, however, delayed and inhibited gland-formation , and suppressed ER expression in the invaginated-lumina l and glandular epithelium at this time. These results indicate that ER expression in these sites is strongly linked with cell proliferating activity. In stromal cells, ER was expressed from PND6 in both groups without any PCNA positive cells, but signi cantly lower values were noted in the OP-treated group up to PND10. Our immunohistochemica l investigation did not reveal any abnormalities in expression of the proto-oncogen e c-fos, mitotic inhibitor p21, or epidermal growth factor antigen, although the apoptotic index in the luminal epithelium was slightly increased in the OP-treated group. These results demonstrate neonatal effects of a high dose of OP, already detectable at PND10, with early and enhanced ER expression, resulting in increase of cell proliferative activity in the luminal epithelium, though expression in the glandular epithelium was suppressed in relation to inhibited gland-genesis . The present study thus suggests that neonatal exposure to high doses of EDCs with estrogenic activity can induce abnormal differentiation in the developing rat uteri via abnormal ER expression and subsequen t alteration of cell proliferating activity.

show abstract

Section: Er (supporting

confidence: 88%

Section: Er (mentioning

confidence: 93%

Neonatal Exposure to p-tert-octylphenol Causes Abnormal Expression of Estrogen Receptor α and Subsequent Alteration of Cell Proliferating Activity in the Developing Donryu Rat Uterus

et al. 2002

View full text Add to dashboard Cite

show abstract

“…The onset of uterine epithelial ER immunostaining was ND 4 in mice (Yamashita et al, 1989) and ND 5 in rats (Table 3, Ohta et al, 1996). ER mRNA was observed starting on ND 7 in rats (Fishman et al, 1996). However, strain differences in the ontogenetic localization of ER were reported in uterine epithelial cells of neonatal BALB/c and CD-1 mice (Bigsby et al, 1990).…”

Section: During Neonatal Development Of the Uterus And Vaginamentioning

confidence: 97%

“…On the day of birth, ER was expressed in epithelial cells of the oviduct, cervix and vagina, but not in the uterus. In contrast, stromal cells expressed ER in all of these organs, including the uterus (Yamashita et al, 1989;Sato et al, 1992Sato et al, , 1996Ohta et al, 1993Ohta et al, , 1996Li, 1994;Fishman et al, 1996). The onset of uterine epithelial ER immunostaining was ND 4 in mice (Yamashita et al, 1989) and ND 5 in rats (Table 3, Ohta et al, 1996).…”

Section: During Neonatal Development Of the Uterus And Vaginamentioning

confidence: 99%

Sex Steroid Hormone Receptors in the Developing Female Reproductive Tract of Laboratory Rodents

Okada¹,

Satō

Ohta

et al. 2005

J. Toxicol. Sci.

View full text Add to dashboard Cite

-Many chemicals released into the environment potentially disrupt the endocrine system in wildlife and humans. Some of these chemicals exhibit estrogenic activity by binding to the estrogen receptors. The developing organism is particularly sensitive to estrogenic chemicals during the critical period in which the induction of long-term changes and persistent molecular alterations in female reproductive tracts occur. Perinatal mouse and rat models can be utilized as indicators for determining the consequences of exposure to exogenous estrogenic agents, including possible xenoestrogens or environmental endocrine disruptors. Estrogen receptors (ER) and estrogen responsive genes, therefore, need to be identified in order to understand the molecular basis of estrogenic actions. Recent identifications of ER subtypes and isoforms make understanding target organ responses to these estrogenic chemicals even more difficult. Indeed, many reports suggest that these chemicals do affect the reproductive and developmental processes of female laboratory rodents that had been perinatally exposed, and that interactions between sex steroid hormone receptors occur. Much information concerning the expression of sex steroid receptors in rodents has been reported concerning the normal development of the Müllerian duct. Thus, accumulated information on the expression of ER subtypes and isoforms as well as that of progesterone and androgen receptors in laboratory rodents is herein reviewed, in addition to the presentation of our own data.

show abstract

“…Thus, the role of endogenous estrogen (17β-estradiol, E2) and its receptor (ER) are very important for uterine growth and differentiation. In normal rats, ER expression in the uterine epithelium appears at various days from PND 7 to PND 15 9 . In female rats, serum FSH (follicle-stimulating hormone) levels rise to a peak at PNDs 15-16 followed by an abrupt nadir, while LH (luteinizing hormone) concentrations are high at PNDs 2-10 followed by gradual decline during sexual maturation; E2 levels also rise to a peak during the first 2 weeks of age 10,11 .…”

Section: Development Of the Female Genital Organs And Profile Of Hormmentioning

confidence: 99%

Toxicologic/carcinogenic Effects of Endocrine Disrupting Chemicals on the Female Genital Organs of Rodents

et al. 2004

View full text Add to dashboard Cite

Toxicologic/carcinogenic effects of some representative endocrine disrupting chemicals (EDCs) having estrogenic activity, such as alkylphenols, on the female genital organs of rodents, especially rats, are reviewed and discussed, focusing on our recent research. Neonatal treatment of high-dose p-tert octylphenol (t-OP, 100 mg/kg s.c. injection every other day from postnatal day 1 (PND 1) to PND 15) induced various long-term persistent irreversible effects on the female reproductive system of Donryu rats, such as lower gonadotropin levels at prepuberty, inhibition of uterine gland genesis, persistent estrus and polycystic ovaries. The result indicates that neonatal high-dose treatment of estrogenic EDCs can affect gonadotropin secretion during the developmental period of sexual maturation with direct masculinization of the hypothalamic function. Exposure limited to the first 5 days after birth (PNDs 1-5) to 100 mg/ kg t-OP, however, caused delayed influence which was characterized by accerelated appearance of atrophic ovary, manifested by early-occurring and long-term continuing persistent estrus after puberty, whereas no abnormalities could be found with regard to growth and differentiation of the reproductive organs and the hypothalamo-pituitary-gonadal control system up to maturation, the influence being caused by delayed modulation of the hypothalamo-pituitary-gonadal control system. The most notable effect on the female reproductive system when normal cycling rats were exposed to high-doses t-OP for 28 days, was disappearance of the estrous cycle, but no clear changes were detected in other parameters such as uterine weight and morphology. These results indicate that the most serious issue with EDCs is the potential effects of prenatal and/or neonatal exposure on rodents. Well or moderately differentiated adenocarcinomas increased in Donryu rats initiated with N-ethyl-N'-nitro-N-nitrosoguanidine, when high-dose t-OP was given subcutaneously during adulthood. Neonatal exposure for PNDs 1-5 to high-dose t-OP also showed promoting effects on uterine adenocarcinoma development. However, in rats given t-OP for PNDs 1-15, uterine tumor malignancy was clearly increased, although there was no significant alteration in the total incidence of adenocarcinomas. The results are very interesting in consideration of the histogenesis of uterine adenocarcinomas. However, maternal exposure to low doses of EDCs such as nonylphenol and bisphenol A at actual human exposure levels by the oral route showed no effects on growth and development of the female reproductive system or uterine carcinogenesis. These results indicate that dietary exposure to low doses of EDCs might not induce any adverse effects on the female genital system in mammals including humans. (J Toxicol Pathol 2004; 17: 69-83)

show abstract

Ontogeny of Estrogen Receptor Messenger Ribonucleic Acid Expression in the Postnatal Rat Uterus1

Cited by 23 publications

References 38 publications

Neonatal Exposure to p-tert-octylphenol Causes Abnormal Expression of Estrogen Receptor α and Subsequent Alteration of Cell Proliferating Activity in the Developing Donryu Rat Uterus

Neonatal Exposure to p-tert-octylphenol Causes Abnormal Expression of Estrogen Receptor α and Subsequent Alteration of Cell Proliferating Activity in the Developing Donryu Rat Uterus

Sex Steroid Hormone Receptors in the Developing Female Reproductive Tract of Laboratory Rodents

Toxicologic/carcinogenic Effects of Endocrine Disrupting Chemicals on the Female Genital Organs of Rodents

Contact Info

Product

Resources

About