Conversion of pregnenolone to progesterone by mouse morulae and blastocysts

Wu, Jia-Rung; Liu, Z. H.

doi:10.1530/jrf.0.0880093

Cited by 8 publications

(1 citation statement)

References 12 publications

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“…There is evidence that rodent blastocysts synthesize P 4 or structurally similar steroids (47)(48)(49) and that gene expression differs in embryo-induced decidua and experimentally induced deciduoma (39). Since our previous results show that Fkbp52 and Pgr are expressed in blastocysts (12), it is possible that P 4 synthesized from blastocysts enhances PR/FKBP52 signaling locally at their sites of apposition in the uterus.…”

Section: Discussionmentioning

confidence: 72%

FKBP52 deficiency–conferred uterine progesterone resistance is genetic background and pregnancy stage specific

Tranguch¹,

Wang²,

Daikoku³

et al. 2007

J. Clin. Invest.

118

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Immunophilin FKBP52 serves as a cochaperone to govern normal progesterone (P 4 ) receptor (PR) function. Using Fkbp52 -/-mice, we show intriguing aspects of uterine P 4 /PR signaling during pregnancy. Implantation failure is the major phenotype found in these null females, which is conserved on both C57BL6/129 and CD1 backgrounds. However, P 4 supplementation rescued implantation and subsequent decidualization in CD1, but not C57BL6/129, null females. Surprisingly, experimentally induced decidualization in the absence of blastocysts failed in Fkbp52 -/-mice on either background even with P 4 supplementation, suggesting that embryonic signals complement uterine signaling for this event. Another interesting finding was that while P 4 at higher than normal pregnancy levels conferred PR signaling sufficient for implantation in CD1 null females, these levels were inefficient in maintaining pregnancy to full term. However, elevating P 4 levels further restored PR signaling to a level optimal for successful term pregnancy with normal litter size. Collectively, the results show that the indispensability of FKBP52 in uterine P 4 /PR signaling is a function of genetic disparity and is pregnancy stage specific. Since there is evidence for a correlation between P 4 supplementation and reduced risks of P 4 -resistant recurrent miscarriages and remission of endometriosis, these findings have clinical implications for genetically diverse populations of women.

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Section: Discussionmentioning

confidence: 72%

FKBP52 deficiency–conferred uterine progesterone resistance is genetic background and pregnancy stage specific

Tranguch¹,

Wang²,

Daikoku³

et al. 2007

J. Clin. Invest.

118

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Preimplantation mouse blastocysts fail to express CYP genes required for estrogen biosynthesis

et al. 1996

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Expression of 3β‐hydroxysteroid dehydrogenase in early bovine embryo development

Chiappe

Lattanzi

Colman‐Lerner

et al. 2002

Molecular Reproduction Devel

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We analyzed the presence of 3 beta-Hydroxysteroid Dehydrogenase/Delta(5-->4)-isomerase enzyme (3 beta-HSD) activity, a key enzyme of the steroid metabolic pathway, the mRNA of this enzyme, and the steroid metabolism in in vitro produced bovine embryos. 3 beta-HSD activity was detected in in vitro matured oocytes (74.4 +/- 1.4%), 1-cell (72.9 +/- 6.1%), 2-cell (61.8 +/- 7.4%), 8-cell (50 +/- 5%), morulae (50.8 +/- 2.6%), blastocysts (94.4 +/- 3%), and hatched blastocysts (100 +/- 0%) meanwhile the 4-cell stage showed a significant reduction (16.7 +/- 4.7%). When total embryonic RNA of different stages was subjected to RT-PCR assays, the mRNA of 3 beta-HSD was found to be present in all developmental stages of in vitro produced bovine embryos, from the oocyte to the blastocyst, with a marked decrease at the 4-cell stage. To determine whether the temporal pattern of enzyme activity was dependent on the maternal to zygotic transition, embryos were incubated in the presence of a transcription inhibitor, alpha-amanitin. The reappearance of the enzyme activity after the 4-cell stage was blocked in alpha-amanitin treated embryos, indicating the requirement of embryonic transcription. On the other hand, the embryonic steroid metabolism was tested by incubating blastocyst with tritiated pregnenolone. Analysis of the metabolites by TLC indicated the production of a compound with a mobility identical to progesterone. These results described the expression of the 3 beta-HSD and the activity of this metabolic enzyme in bovine oocytes and preimplantation embryos, suggesting that steroids may act as autocrine effectors on preimplantation embryo development.

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Conversion of pregnenolone to progesterone by mouse morulae and blastocysts

Cited by 8 publications

References 12 publications

FKBP52 deficiency–conferred uterine progesterone resistance is genetic background and pregnancy stage specific

FKBP52 deficiency–conferred uterine progesterone resistance is genetic background and pregnancy stage specific

Preimplantation mouse blastocysts fail to express CYP genes required for estrogen biosynthesis

Expression of 3β‐hydroxysteroid dehydrogenase in early bovine embryo development

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