Trophoblastic Giant Cells in Placentas of Rats and Mice and Their Probable Role in Steroid-Hormone Production

Deane, Helen Wendler; Rubin, Betty L.; Driks, Ellen C.; Lobel, Bertha L.; Leipsner, George

doi:10.1210/endo-70-3-407

Cited by 127 publications

(35 citation statements)

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“…the interstitial parts of the testes (Berlin & Ullberg, 1963) and the follicles and CL, the decidual uptake also seen in mice at late gestation may be compared with that of 3j8-hydroxysteroid dehydrogenase described earlier in rats and mice (Deane et al, 1962;Botte et al, 1966). Appelgren (1967) (Harris, 1927).…”

Section: Decidua and Placentaementioning

confidence: 86%

Possible Mechanisms of Cadmium Fetotoxicity in Golden Hamsters and Mice: Uptake by the Embryo, Placenta and Ovary

Dencker¹

1975

Reproduction

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Summary. Pregnant golden hamsters and mice of different gestational ages were injected intravenously with 109CdCl2. The whole animal or the uterus and embryos were submitted to autoradiography. Cadmium administered on the 8th day accumulated in the primitive gut of the embryos. No cadmium was detected in the embryos after administration on or after the 9th day (hamster) and 11th day (mouse). This finding can be explained by the ability of cadmium to pass from the yolk-sac cavity into the primitive gut (where it is absorbed) before the closure of the vitelline duct but not later. This uptake by the embryo might explain the severe malformations produced by cadmium given on the 8th day as compared with the 9th day in the hamster. Cadmium is also heavily accumulated in the decidua (mainly the antimesometrial part), the yolk sac, the ectoplacental cone, and later in the chorioallantoic placenta\p=m-\possiblydisturbing the maternal-embryonic relationship and fetal nutrition. A high accumulation in the CL and the follicles and in the pituitary may also disturb reproductive function.

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Section: Decidua and Placentaementioning

confidence: 86%

Possible Mechanisms of Cadmium Fetotoxicity in Golden Hamsters and Mice: Uptake by the Embryo, Placenta and Ovary

Dencker¹

1975

Reproduction

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“…The placenta is the only major steroidproducing organ which develops in SF-1 -/-mice. Placental steroidogenesis takes place in trophoblast-derived cells (19)(20)(21). These cells originate in fetal tissues and express P450scc (19), a known target for SF-1 regulation in vitro (4).…”

Section: Sf-1-deficient Mice Lack Adrenal Glands and Gonadsmentioning

confidence: 99%

Mice deficient in the orphan receptor steroidogenic factor 1 lack adrenal glands and gonads but express P450 side-chain-cleavage enzyme in the placenta and have normal embryonic serum levels of corticosteroids.

Sadovsky

Crawford

Woodson

et al. 1995

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

428

249

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The orphan nuclear receptor steroidogenic factor 1 (SF-1) is expressed in the adrenal cortex and gonads and regulates the expression of several P450 steroid hydroxylases in vitro. We examined the role of SF-i in the adrenal glands and gonads in vivo by a targeted disruption of the mouse SF-1 gene. All SF-i-deficient mice died shortly after delivery. Their adrenal glands and gonads were absent, and persistent Mullerian structures were found in all genotypic males. While serum levels of corticosterone in SF-1-deficient mice were diminished, levels of adrenocorticotropic hormone (ACTH) were elevated, consistent with intact pituitary corticotrophs. Intrauterine survival of SF-i-deficient mice appeared normal, and they had normal serum level of corticosterone and ACTH, probably reflecting transplacental passage of maternal steroids. We tested whether SF-i is required for P450 side-chain-cleavage enzyme (P450scc) expression in the placenta, which expresses both SF-1 and P450scc, and found that in contrast to its strong activation of the P450scc gene promoter in vitro, the absence of SF-1 had no effect on P450scc mRNA levels in vivo. Although the region targeted by our disruption is shared by SF-1 and by embryonal long terminal repeat-binding protein (ELP), a hypothesized alternatively spliced product, we believe that the observed phenotype reflects absent SF-1 alone, as PCR analysis failed to detect ELP transcripts in any mouse tissue, and sequences corresponding to ELP are not conserved across species. These results confirm that SF-1 is an important regulator of adrenal and gonadal development, but its regulation of steroid hydroxylase expression in vivo remains to be established.

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“…In addition, we On the following day, our routine procedure was to treat the specimens by methods modified only slightly from those employed by Deane, Rubin, Driks, Lobel & Leipsner (1962) and Rubin et al (1963) (see Deane, Hay, Moor, Rowson & Short, 1966). The coverslips were transferred without being warmed to redistilled acetone at 4°C , for 5 min, and then immersed in two changes of cold 0-1 M-phosphate buffer, pH 7-5, for a total of 5 min, to remove free lipids and soluble endogenous substrates.…”

Section: Introductionmentioning

confidence: 99%

Attempts to Demonstrate 3 - And 17 -Hydroxy-Steroid Dehydrogenases Histochemically in the Testes of the Stallion, Boar, Ram and Bull

Hay¹,

Deane²

1966

Reproduction

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Trophoblastic Giant Cells in Placentas of Rats and Mice and Their Probable Role in Steroid-Hormone Production

Cited by 127 publications

References 0 publications

Possible Mechanisms of Cadmium Fetotoxicity in Golden Hamsters and Mice: Uptake by the Embryo, Placenta and Ovary

Possible Mechanisms of Cadmium Fetotoxicity in Golden Hamsters and Mice: Uptake by the Embryo, Placenta and Ovary

Mice deficient in the orphan receptor steroidogenic factor 1 lack adrenal glands and gonads but express P450 side-chain-cleavage enzyme in the placenta and have normal embryonic serum levels of corticosteroids.

Attempts to Demonstrate 3 - And 17 -Hydroxy-Steroid Dehydrogenases Histochemically in the Testes of the Stallion, Boar, Ram and Bull

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