The Effect of Estrogens on the Ovary of the Hypophysectomized Rat

Payne, R. W.; Hellbaum, Arthur A.

doi:10.1210/endo-57-2-193

Cited by 50 publications

(22 citation statements)

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“…The idea of a direct steroid effect is further supported by the observation that, when oestrogen is co-administered with DHT (Table 2), the expected decrease in the number of ovulations failed to occur. Other investigators (Payne & Hellbaum, 1955;McNatty et ai, 1979;Richards & Kersey, 1979;Braw et ai, 1981) have likewise concluded that adequate oestrogen production is essential to follicular development.…”

Section: Discussionmentioning

confidence: 94%

Effect of dihydrotestosterone on the growth and function of ovarian follicles in intact immature female rats primed with PMSG

Conway

Mahesh²,

Mills³

1990

Reproduction

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Section: Discussionmentioning

confidence: 94%

Effect of dihydrotestosterone on the growth and function of ovarian follicles in intact immature female rats primed with PMSG

Conway

Mahesh²,

Mills³

1990

Reproduction

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“…At this stage, proliferating granulosa cells acquire luteinizing hormone receptors and the subsequent luteinizing hormone surge triggers granulosa cells of preovulatory follicles to exit the cell cycle (Robker and Richards, 1998). Estrogen maintains granulosa cells in experimental mice (Britt et al, 2002) and stimulates granulosa cell proliferation in small preantral follicles in hypophysectomized rats (Payne and Hellbaum, 1955); however, the molecular mechanisms underlying the estrogen regulation of cell proliferation remain unclear (Britt et al, 2002). The estrogen-deficient aromatase knockout (ArKO) mouse model has been useful for studies of the requirement for estrogen function in the ovary (Miller et al, 2007b).…”

Section: Introductionmentioning

confidence: 99%

Estrogen deficiency reversibly induces telomere shortening in mouse granulosa cells and ovarian aging in vivo

Bayne

Jones

et al. 2011

Protein Cell

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Estrogen is implicated as playing an important role in aging and tumorigenesis of estrogen responsive tissues; however the mechanisms underlying the mitogenic actions of estrogen are not fully understood. Here we report that estrogen deficiency in mice caused by targeted disruption of the aromatase gene results in a significant inhibition of telomerase maintenance of telomeres in mouse ovaries in a tissue-specific manner. The inhibition entails a significant shortening of telomeres and compromised proliferation in the follicular granulosa cell compartment of ovary. Gene expression analysis showed decreased levels of proto-oncogene c-Myc and the telomerase catalytic subunit, telomerase reverse transcriptase (TERT), in response to estrogen deficiency. Estrogen replacement therapy led to increases in TERT gene expression, telomerase activity, telomere length and ovarian tissue growth, thereby reinstating ovary development to normal in four weeks. Our data demonstrate for the first time that telomere maintenance is the primary mechanism mediating the mitogenic effect of estrogen on ovarian granulosa cell proliferation by upregulating the genes of c-Myc and TERT in vivo. Estrogen deficiency or over-activity may cause ovarian tissue aging or tumorigenesis, respectively, through estrogen regulation of telomere remodeling.

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“…Androgens originating in the theca cells feed granulosa cells to produce estradiol [1]. In turn, estradiol stimulates follicular growth, increases ovarian weight, enhances the mitotic index of granulosa cells, and inhibits granulosa cell apoptosis [2][3][4][5]. The expression of AR in granulosa cells of various species of mammals [6][7][8][9][10] makes these cells responsive to androgens.…”

Section: Introductionmentioning

confidence: 99%

Androstenedione Interferes in Luteal Regression by Inhibiting Apoptosis and Stimulating Progesterone Production1

Goyeneche

Calvo

Gibori

et al. 2002

Biology of Reproduction

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Androgens, in concert with lactogenic hormones, contribute to the maintenance of function of the corpus luteum (CL) in pregnant rats. Whereas some of the androgenic actions in the CL are clearly mediated by intracrine conversion to estrogen, pure androgenic effects are also implicated in the regulation of this transient endocrine gland. In this report, we have established, to our knowledge for the first time, the expression of androgen receptor (AR) mRNA and protein throughout gestation in the rat CL. We have found that the AR remains expressed in the CL of gestation on Day 4 postpartum and becomes expressed in the newly formed CL after postpartum ovulation. An AR immunoreactive protein was identified in the CL of pregnancy as well as in prostate and epididymis, which were used as positive controls. The luteal AR protein had mainly nuclear localization, yet some diffuse cytoplasmic staining was also observed. Moreover, we have established that androstenedione, the main circulating androgen in pregnant rats, significantly reduces the decline in luteal weight observed during postpartum structural regression. This effect was correlated with a decrease in the number of cells undergoing apoptosis and with enhanced levels of circulating progesterone. In addition, in vivo administration of androstenedione delayed the occurrence of DNA fragmentation in postpartum CL incubated in serum-free conditions. Finally, we have shown that the interference with apoptosis in vitro elicited by androstenedione is accompanied by an increased capacity of the CL to secrete progesterone. In summary, the results of this study have established that the rat CL expresses AR throughout pregnancy and after parturition, and they have defined a potential role for androstenedione in opposing postpartum luteal regression through inhibition of apoptosis and stimulation of progesterone production.

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The Effect of Estrogens on the Ovary of the Hypophysectomized Rat

Cited by 50 publications

References 0 publications

Effect of dihydrotestosterone on the growth and function of ovarian follicles in intact immature female rats primed with PMSG

Effect of dihydrotestosterone on the growth and function of ovarian follicles in intact immature female rats primed with PMSG

Estrogen deficiency reversibly induces telomere shortening in mouse granulosa cells and ovarian aging in vivo

Androstenedione Interferes in Luteal Regression by Inhibiting Apoptosis and Stimulating Progesterone Production1

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