Age-Dependent Participation of the Adenohypophysis and Adrenal Cortex in the Estrogenic Response of the Quail Oviduct

Laugier, Christian; Sonnenschein, Carlos; Brard, E

doi:10.1210/endo-106-5-1392

Cited by 12 publications

(4 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As we have demonstrated using castrated and hypophysectomized quail, such treat¬ ments have overestimated the role of oestradiol (Laugier, Sandoz, Brard & Sonnenschein, 1978;Laugier, Sonnenschein & Brard, 1980). In previous reports we have shown that in castrated quail oestradiol benzoate (10 pg daily) reproduces condi¬ tions compatible with normal oestrogen stimulation (Laugier, Claustrat & Brard, 1978) and induces cell proliferation, ciliogenesis and tubular gland forma¬ tion Sandoz et al 1975).…”

Section: Discussionmentioning

confidence: 87%

Development of the oviduct in quail during sexual maturation in relation to plasma concentrations of oestradiol and progesterone

Pageaux¹,

Laugier²,

Pal³

et al. 1984

Journal of Endocrinology

Self Cite

View full text Add to dashboard Cite

The macromolecular content (DNA, soluble proteins and ovalbumin) of the magnum and the plasma concentrations of oestradiol and progesterone were studied during sexual development of the Japanese quail. Rapid growth and differentiation of the magnum began between 21 and 28 days of age and rapidly reached the laying stage in about 20 days. This rapid change in magnum size occurred in a stepwise manner: cellular proliferation was observed first, followed by the synthesis and accumulation of specific proteins. Just before and during magnum growth, plasma oestradiol and progesterone concentrations followed different patterns: the initiation of epithelial cell proliferation was preceded by a sharp decrease in plasma progesterone. Maximum cell division occurred while plasma progesterone levels continued to decrease slightly; at the same time, oestradiol increased from 0.098 to 0.453 nmol/l. The decrease and finally the cessation of cell proliferation and the concomitant increase in ovalbumin concentration were related to almost constant levels of plasma oestradiol and increasing levels of plasma progesterone. Further development of the magnum (above 2.3 g weight) involving only the accumulation of secretory products was associated with an increased value of plasma progesterone. These data are consistent with the hypothesis that there are multiple hormonal signals controlling cell proliferation and synthesis of egg-white proteins in the oviduct. Progesterone may be one of the key signals that regulates the initiation of oviduct growth in the quail.

show abstract

Section: Discussionmentioning

confidence: 87%

Development of the oviduct in quail during sexual maturation in relation to plasma concentrations of oestradiol and progesterone

Pageaux¹,

Laugier²,

Pal³

et al. 1984

Journal of Endocrinology

Self Cite

View full text Add to dashboard Cite

show abstract

“…In the past, we explored the role of E2 on the proliferation of its target cells through the direct positive (Sonnenschein and Soto, 1980) and indirect positive (Sonnenschein and Soto, 1977;Laugier et al, 1980;Schatz et al, 1984) working hypotheses. We have recently begun to explore the mechanism of estrogen action on cellular proliferation by testing the indirect and direct negative working hypothesis .…”

mentioning

confidence: 99%

“…The mechanism by which estrogens regulate the proliferation of cells in organs of the reproductive tract of vertebrates has not been altogether defined (Sirbasku and Benson, 1979;Sonnenschein and Soto, 1980;Stack and Gorski, 1984;Spolski et al, 1985). In the past, we explored the role of E2 on the proliferation of its target cells through the direct positive (Sonnenschein and Soto, 1980) and indirect positive (Sonnenschein and Soto, 1977;Laugier et al, 1980;Schatz et al, 1984) working hypotheses. We have recently begun to explore the mechanism of estrogen action on cellular proliferation by testing the indirect and direct negative working hypothesis .…”

mentioning

confidence: 99%

On the role of 17 alpha‐estradiol and 17 beta‐estradiol in the proliferation of MCF7 and T47D‐A11 human breast tumor cells

Papendorp

Schatz

Soto

et al. 1985

Journal Cellular Physiology

View full text Add to dashboard Cite

A comparative study of the proliferative effect of 17 beta-estradiol and 17 alpha-estradiol on human estrogen-sensitive cell lines was performed. When using charcoal-dextran stripped human female sera-supplemented media the administration of the hormones, 17 alpha-estradiol at 3 X 10(-10)M, and 17 beta-estradiol at 3 X 10(-11)M, resulted in a ten-fold increase in cell yield when compared with non-estrogen supplemented controls after cells were grown for periods between 10 to 14 days. No significant metabolization of 17 alpha-estradiol into 17 beta-estradiol occurred as measured by the E2 levels in the supernatants of the cell culture flasks. Increased concentrations of 17 beta-estradiol and 17 alpha-estradiol added to the media bathing C7MCF7-173 cells resulted in a triggering of a partially successful shut-off effect; this phenomenon was not observed with T47D-All cells. These results are compatible with predictions stemming from the indirect and direct negative working hypothesis for the regulation of cell proliferation.

show abstract

“…The central argument postulated for mammals by Jensen's group and later extended to birds and other phyla suggests that the full response of these target tissues to the administration of estrogen is direct, regardless of the parameter measured (5,6). Among the many markers that have been linked to this putatively direct effect, the more thoroughly studied are (i) the induction of certain proteins [ovalbumin, prolactin, creatine kinase, progesterone receptors (progestophilins), and others] (7-15), (ii) the inhibition of the synthesis of gonadotropins and other cell proteins (16,17), and (iii) the proliferative response of the uterus (18)(19)(20), vagina (21), mammary glands (22), bird oviduct (23,24), and a number of estrogen-sensitive tumors (25) and cultured cell lines (13)(14)(15)(26)(27)(28).…”

mentioning

confidence: 99%

Mechanism of estrogen action: Indirect effect of estradiol-17β on proliferation of quail oviduct cells

Laugier¹,

Pageaux²,

Soto³

et al. 1983

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

View full text Add to dashboard Cite

Experimental data were collected to test whether the effect of estrogens required a direct action of the steroid on their target cells for induction of (i) cell multiplication and (ii) celltype-specific protein synthesis. Ovariectomized quails were perfused for 24 hr with several doses of estradiol-17.8 (E2) (0.05-6.8 ng/min) through either thejugular vein or the portal vein. E2 plasma concentrations increased progressively when the perfusion rate through thejugular vein was 0.5 ng/min and higher. With the portal vein, by contrast, E2 plasma concentrations increased over the concentration in unperfused ovariectomized animals only when the perfusion rate was above 2 ng/min. An increase in DNA concentration per oviduct was observed regardless of the route of administration and the rate of perfusion, starting at 0.5 ng/min. Nuclear estrophilins increased when E2 was perfused through the jugular vein at rates of 0.5 ng/min or greater. This same parameter was not increased in oviducts of quail perfused through the portal vein even at a perfusion rate of 2.0 ng/min. Progestophilins were induced in the oviducts of quail perfused through thejugular vein at rates of 2 ng/min and above; on the other hand, progestophilins were induced in birds perfused through the portal vein at rates above 2 ng/min. Ovalbumin was not induced in quail oviducts at any rate and route of perfusion. The induction of the synthesis of cell-type-specific protein (progestophilins, in this case) seems to require, however, the direct action of E2. The E2 concentrations effecting the induction of progestophilins were higher than those necessary to effect the proliferation of oviduct cells. These results suggest that the E2 effect on cell proliferation is indirect, it involves an intermediary step at the liver, and it does not require increased concentration of nuclear estrophilins.An extensive literature regarding the mechanism of estrogen action in the oviduct of birds is available (1-4). The central argument postulated for mammals by Jensen's group and later extended to birds and other phyla suggests that the full response of these target tissues to the administration of estrogen is direct, regardless of the parameter measured (5,6). Among the many markers that have been linked to this putatively direct effect, the more thoroughly studied are (i) the induction of certain proteins [ovalbumin, prolactin, creatine kinase, progesterone receptors (progestophilins), and others] (7-15), (ii) the inhibition of the synthesis of gonadotropins and other cell proteins (16,17), and (iii) the proliferative response of the uterus (18)(19)(20), vagina (21), mammary glands (22), bird oviduct (23, 24), and a number of estrogen-sensitive tumors (25) and cultured cell lines (13)(14)(15)(26)(27)(28).Despite the abundant bibliography on these subjects, whether the effect of estrogens on cell multiplication is exerted through a direct or indirect pathway remains a controversial subject (21,22,(28)(29)(30). The latter possibility implies that at least one interme...

show abstract

Age-Dependent Participation of the Adenohypophysis and Adrenal Cortex in the Estrogenic Response of the Quail Oviduct

Cited by 12 publications

References 13 publications

Development of the oviduct in quail during sexual maturation in relation to plasma concentrations of oestradiol and progesterone

Development of the oviduct in quail during sexual maturation in relation to plasma concentrations of oestradiol and progesterone

On the role of 17 alpha‐estradiol and 17 beta‐estradiol in the proliferation of MCF7 and T47D‐A11 human breast tumor cells

Mechanism of estrogen action: Indirect effect of estradiol-17β on proliferation of quail oviduct cells

Contact Info

Product

Resources

About