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Hiroshi Kanagawa - One of the best experts on this subject based on the ideXlab platform.

  • A Delayed-Implantation-associated protein prevents resumption of DNA synthesis by the trophectoderm of Delayed-implanting mouse blastocysts in vitro.
    The Journal of veterinary medical science, 1998
    Co-Authors: Seiji Katagiri, Basil Ho Yuen, Hiroshi Kanagawa, Yoshiyuki Takahashi, Young S. Moon
    Abstract:

    Objective of this study was to determine the ability of a Delayed-Implantation-associated protein (MW 170,000, DIAP170K) to inhibit DNA synthesis by mouse blastocysts. Mice were ovariectomized on day 3 of pregnancy and treated with daily injections with 1 mg progesterone till day 7 to induce Delayed Implantation. Blastocysts were collected on day 8 with or without a single injection of 25 ng estradiol-17 beta on day 7 that activates blastocyst metabolisms (activated blastocysts and Delayed-implanting blastocysts respectively). DNA synthesis was determined by measuring [3H]thymidine incorporation by blastocysts. DIAP170K at 10 micrograms/m/ suppressed resumption of DNA synthesis by Delayed-implanting blastocysts and suppression was maximal at 50 micrograms/m/. However, DIAP170K did not affect DNA synthesis by blastocysts obtained on day 5 of pregnancy (normal blastocysts) and activated blastocysts. Resumption of DNA synthesis in the inner cell mass (ICM) and trophectoderm from Delayed-implanting blastocysts was then separately assessed. DNA synthesis resumed in the trophectoderm of intact blastocysts during 24-hr culture but not in the trophectoderm cultured apart from the ICM. DIAP170K inhibited the resumption of DNA synthesis by the trophectoderm of intact Delayed-implanting blastocysts but did not affect DNA synthesis by the ICM. In conclusion, DIAP170K inhibits resumption of DNA synthesis by trophectoderm of Delayed-implanting blastocysts. This action of DIAP170K may play a central role in maintaining, but not achieving, dormancy of DNA synthesis by Delayed-implanting blastocysts in mice.

  • Separation of a 170‐K Delayed‐Implantation‐Associated Protein With Inhibitory Activity on Trophoblast Outgrowth and RNA Synthesis by Mouse Embryo
    American journal of reproductive immunology (New York N.Y. : 1989), 1994
    Co-Authors: Seiji Katagiri, Basil Ho Yuen, Young S. Moon, Yoshyuki Takahashi, Hiroshi Kanagawa
    Abstract:

    PROBLEM: To screen the uterine protein responsible for embryonic dormancy associated with Delayed Implantation. METHOD: Uterine protein extracts and sera from mice in which Delayed Implantation had been induced and those from pregnant mice were separated by three steps of chromatography and SDS-PAGE by monitoring an inhibitory activity on trophoblast outgrowth. The presence of the separated protein in the uterine luminal fluid was assessed. Effect of the protein on cell proliferation and RNA synthesis by blastocysts were assessed. RESULTS: A 170-K protein was found in the uterine tissue as well as uterine luminal fluid associated with Delayed Implantation. The 170-K protein suppressed RNA synthesis by approximately 50% and cell proliferation in blastocysts. CONCLUSION: A 170-K protein is secreted into the uterine lumen during Delayed Implantation period. The ability of 170-K protein to suppress RNA synthesis and cell proliferation may play a role in regulation of embryonic dormancy associated with Delayed Implantation.

  • Morphological characteristics of the ovary, uterus and embryo during the Delayed Implantation period in the Hokkaido brown bear (Ursus arctos yesoensis)
    Journal of Reproduction and Development, 1993
    Co-Authors: Toshio Tsubota, Hiroshi Kanagawa
    Abstract:

    Ovaries having corpora lutea and uteri of 6 female Hokkaido brown bears (Ursus arctos yesoensis), which were legally killed by hunters from October to December in Hokkaido, Japan, were examined macroscopically and histologically. Four of the 6 female bears had unimplanted embryos in the uterine lumen during the period of Delayed Implantation between October 19 and November 20. Ovaries of bears which had unimplanted embryos contained the corpora lutea with extensive vacuolation or numerous granules in the cytoplasm of luteal cells. These bears had well-developed uterine glands which had tall epithelial cells with vacuoles in the cytoplasm of glandular cells and coagula in the glandular lumina. It is concluded that Hokkaido brown bears exhibit obligate Delayed Implantation and that this period of Delayed Implantation continues at least until late November.

Rodney A. Mead - One of the best experts on this subject based on the ideXlab platform.

  • spatiotemporal expression of cyclooxygenase 1 and cyclooxygenase 2 during Delayed Implantation and the periImplantation period in the western spotted skunk
    Biology of Reproduction, 1999
    Co-Authors: Sanjoy K Das, S K Dey, J Wang, Rodney A. Mead
    Abstract:

    Embryonic development in the western spotted skunk is arrested after blastocyst formation for about 200 days. This developmental arrest is believed to be due to insufficiency of uterine conditions to support continuous development. Implantation and decidualization are defective in cyclooxygenase 2 (Cox2)-, but not Cox1-, deficient mice. We therefore used Northern and in situ hybridization to investigate changes in uterine expression of Cox1 and Cox2 genes during various stages of pregnancy in the spotted skunk. Cox1 was constitutively expressed at all stages of pregnancy examined, but it did exhibit localized up-regulation in the trophoblast and necks of uterine glands at early Implantation sites. Cox2 expression was highly regulated with little or no expression during Delayed Implantation. Cox2 expression was first detected in the uterus and trophoblast prior to blastocyst attachment and remained detectable for 5-6 days after blastocyst attachment. Cox2 expression was also localized in the luminal and glandular epithelia of uterine segments located between Implantation chambers. Changes in Cox expression were not correlated with the abrupt increase in uterine weight that occurs simultaneously with renewed embryonic development but was correlated with an influx of serum proteins into the uterus observed in a previous study.

  • Changes in uterine estrogen and progesterone receptors during Delayed Implantation and early Implantation in the spotted skunk.
    Biology of reproduction, 1995
    Co-Authors: Rodney A. Mead, Victor P. Eroschenko
    Abstract:

    Although the exact cause(s) of embryonic diapause in the western spotted skunk and other carnivores remains unknown, it has been hypothesized that it may be due to levels of ovarian hormone secretion that are insufficient to promote a uterine environment conducive to continuous embryonic development and Implantation. Immunocytochemistry was used to determine whether changes in abundance or distribution of estrogen receptors (ER) and progesterone receptors (PR) may be associated with the cessation or renewal of embryonic development. Thirty pregnant skunks were killed during Delayed Implantation and periImplantation periods. ER and PR were detected in luminal and glandular epithelium, endometrial stroma, vasculature, and myometrium of the uterus during the period of Delayed Implantation. There was a significant reduction of both ER and PR receptors during the periImplantation period. The most pronounced change was the complete loss or reduction in staining intensity for PR and ER in the luminal epithelium during the first 2-3 days after Implantation. These findings suggest that the failure of skunk blastocysts to undergo continuous development and implant without a prolonged period of diapause is not the result of an insufficient number of ER or PR in the uterus. The data also indicate that renewed embryonic development and Implantation is not associated with an increase in these uterine steroid receptors.

Seiji Katagiri - One of the best experts on this subject based on the ideXlab platform.

  • A Delayed-Implantation-associated protein prevents resumption of DNA synthesis by the trophectoderm of Delayed-implanting mouse blastocysts in vitro.
    The Journal of veterinary medical science, 1998
    Co-Authors: Seiji Katagiri, Basil Ho Yuen, Hiroshi Kanagawa, Yoshiyuki Takahashi, Young S. Moon
    Abstract:

    Objective of this study was to determine the ability of a Delayed-Implantation-associated protein (MW 170,000, DIAP170K) to inhibit DNA synthesis by mouse blastocysts. Mice were ovariectomized on day 3 of pregnancy and treated with daily injections with 1 mg progesterone till day 7 to induce Delayed Implantation. Blastocysts were collected on day 8 with or without a single injection of 25 ng estradiol-17 beta on day 7 that activates blastocyst metabolisms (activated blastocysts and Delayed-implanting blastocysts respectively). DNA synthesis was determined by measuring [3H]thymidine incorporation by blastocysts. DIAP170K at 10 micrograms/m/ suppressed resumption of DNA synthesis by Delayed-implanting blastocysts and suppression was maximal at 50 micrograms/m/. However, DIAP170K did not affect DNA synthesis by blastocysts obtained on day 5 of pregnancy (normal blastocysts) and activated blastocysts. Resumption of DNA synthesis in the inner cell mass (ICM) and trophectoderm from Delayed-implanting blastocysts was then separately assessed. DNA synthesis resumed in the trophectoderm of intact blastocysts during 24-hr culture but not in the trophectoderm cultured apart from the ICM. DIAP170K inhibited the resumption of DNA synthesis by the trophectoderm of intact Delayed-implanting blastocysts but did not affect DNA synthesis by the ICM. In conclusion, DIAP170K inhibits resumption of DNA synthesis by trophectoderm of Delayed-implanting blastocysts. This action of DIAP170K may play a central role in maintaining, but not achieving, dormancy of DNA synthesis by Delayed-implanting blastocysts in mice.

  • Separation of a 170‐K Delayed‐Implantation‐Associated Protein With Inhibitory Activity on Trophoblast Outgrowth and RNA Synthesis by Mouse Embryo
    American journal of reproductive immunology (New York N.Y. : 1989), 1994
    Co-Authors: Seiji Katagiri, Basil Ho Yuen, Young S. Moon, Yoshyuki Takahashi, Hiroshi Kanagawa
    Abstract:

    PROBLEM: To screen the uterine protein responsible for embryonic dormancy associated with Delayed Implantation. METHOD: Uterine protein extracts and sera from mice in which Delayed Implantation had been induced and those from pregnant mice were separated by three steps of chromatography and SDS-PAGE by monitoring an inhibitory activity on trophoblast outgrowth. The presence of the separated protein in the uterine luminal fluid was assessed. Effect of the protein on cell proliferation and RNA synthesis by blastocysts were assessed. RESULTS: A 170-K protein was found in the uterine tissue as well as uterine luminal fluid associated with Delayed Implantation. The 170-K protein suppressed RNA synthesis by approximately 50% and cell proliferation in blastocysts. CONCLUSION: A 170-K protein is secreted into the uterine lumen during Delayed Implantation period. The ability of 170-K protein to suppress RNA synthesis and cell proliferation may play a role in regulation of embryonic dormancy associated with Delayed Implantation.

Victor P. Eroschenko - One of the best experts on this subject based on the ideXlab platform.

  • Changes in uterine estrogen and progesterone receptors during Delayed Implantation and early Implantation in the spotted skunk.
    Biology of reproduction, 1995
    Co-Authors: Rodney A. Mead, Victor P. Eroschenko
    Abstract:

    Although the exact cause(s) of embryonic diapause in the western spotted skunk and other carnivores remains unknown, it has been hypothesized that it may be due to levels of ovarian hormone secretion that are insufficient to promote a uterine environment conducive to continuous embryonic development and Implantation. Immunocytochemistry was used to determine whether changes in abundance or distribution of estrogen receptors (ER) and progesterone receptors (PR) may be associated with the cessation or renewal of embryonic development. Thirty pregnant skunks were killed during Delayed Implantation and periImplantation periods. ER and PR were detected in luminal and glandular epithelium, endometrial stroma, vasculature, and myometrium of the uterus during the period of Delayed Implantation. There was a significant reduction of both ER and PR receptors during the periImplantation period. The most pronounced change was the complete loss or reduction in staining intensity for PR and ER in the luminal epithelium during the first 2-3 days after Implantation. These findings suggest that the failure of skunk blastocysts to undergo continuous development and implant without a prolonged period of diapause is not the result of an insufficient number of ER or PR in the uterus. The data also indicate that renewed embryonic development and Implantation is not associated with an increase in these uterine steroid receptors.

Zeng-ming Yang - One of the best experts on this subject based on the ideXlab platform.

  • hb egf regulates prss56 expression during mouse decidualization via egfr erk egr2 signaling pathway
    Journal of Endocrinology, 2017
    Co-Authors: Jie Liu, Fei Gao, Yuefang Liu, Haiting Dou, Jiaqi Yan, Zongmin Fan, Zeng-ming Yang
    Abstract:

    Embryo Implantation and decidualization are key steps for successful reproduction. Although numerous factors have been identified to be involved in embryo Implantation and decidualization, the mechanisms underlying these processes are still unclear. Based on our preliminary data, Prss56, a trypsin-like serine protease, is strongly expressed at Implantation site in mouse uterus. However, the expression, regulation and function of Prss56 during early pregnancy are still unknown. In mouse uterus, Prss56 is strongly expressed in the subluminal stromal cells at Implantation site on day 5 of pregnancy compared to inter-Implantation site. Under Delayed Implantation, Prss56 expression is undetected. After Delayed Implantation is activated by estrogen, Prss56 is obviously induced at Implantation site. Under artificial decidualization, Prss56 signal is seen at the primary decidual zone at the initial stage of artificial decidualization. When stromal cells are induced for in vitro decidualization, Prss56 expression is significantly elevated. Dtprp expression under in vitro decidualization is suppressed by Prss56 siRNA. In cultured stromal cells, HB-EGF markedly stimulates Prss56 expression through EGFR/ERK pathway. Based on promoter analysis, we also showed that Egr2 is involved in Prss56 regulation by HB-EGF. Collectively, Prss56 expression at Implantation site is modulated by HB-EGF/EGFR/ERK signaling pathway and involved in mouse decidualization.

  • effects of androgen on embryo Implantation in the mouse Delayed Implantation model
    Fertility and Sterility, 2008
    Co-Authors: Hong-lu Diao, Zeng-ming Yang, Hui-ning Tan, Wei Lei, Weng-bo Deng
    Abstract:

    National Basic Research Program of China [2006CB504005, 2006CB944009]; Chinese National Natural Science Foundation [30330060, 30570198]

  • Effects of androgen on embryo Implantation in the mouse Delayed-Implantation model.
    Fertility and sterility, 2007
    Co-Authors: Hong-lu Diao, Hui-ning Tan, Wei Lei, Weng-bo Deng, Zeng-ming Yang
    Abstract:

    To examine the effects of androgen on Implantation and decidualization in the mouse Delayed-Implantation model. Experimental animal study. University research laboratory. Sexually mature female mice (Kunming White strain). Delayed and activated Implantation; pseudopregnancy; embryo transfer (ET); E(2) assay; inhibitor. Effects of androgen on embryo Implantation were determined by treating the mice under Delayed Implantation with different doses of testosterone propionate (TP); the effects of androgen on the expression of Implantation-related genes were examined by in situ hybridization. Delayed Implantation could be initiated by TP. Dihydrotestosterone was also able to initiate Implantation in the Delayed-Implantation model. The Implantation window could be maintained for at least 48 hours by 5 mg TP per mouse. Prostaglandin endoperoxide synthase 2 (Ptgs2) and microsomal prostaglandin E synthase (mPtges) were aberrantly expressed in mouse uterus at Implantation sites after Delayed Implantation was activated by high doses of TP. A low dose of TP led to a delay in embryo Implantation, but a high dose caused aberrant expression of both Ptgs2 and mPtges at the Implantation site. It is possible that high doses of TP may disturb peri-Implantation development or may be involved in early pregnancy loss by disturbing the uterine prostaglandin system.

  • Basigin expression and hormonal regulation in the rat uterus during the peri-Implantation period
    Reproduction (Cambridge England), 2002
    Co-Authors: Lj Xiao, Kenji Kadomatsu, Takashi Muramatsu, Hl Diao, Nz Ding, Zeng-ming Yang
    Abstract:

    Basigin is essential for fertilization and Implantation. The aim of this study was to determine the expression and hormonal regulation of the basigin gene in the rat uterus during the peri-Implantation period. Basigin mRNA was localized strongly in the luminal epithelium on day 1 of pregnancy and gradually decreased to a basal concentration from day 3 to day 5 of pregnancy. Basigin mRNA and protein were expressed strongly in the implanting blastocyst and primary decidua on day 6 of pregnancy. A similar expression pattern was also induced in the uterus after Delayed Implantation was terminated by oestrogen treatment and the embryo implanted, whereas expression was not detected during Delayed Implantation. Basigin expression was not detected on day 6 of pseudopregnancy. Basigin mRNA was expressed strongly in the decidua on days 7 and 8 of pregnancy. Furthermore, both basigin mRNA and protein were induced in the decidua during artificial decidualization. In addition, oestrogen stimulated strong expression of basigin mRNA in the uterine epithelium of ovariectomized rats. These findings indicate that basigin may play a role during Implantation and decidualization in rats.