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Identification of Sites of STAT3 Action in the Female Reproductive Tract through Conditional Gene Deletion

The STAT3 transcription factor is a pleiotropic transducer of signalling by hormones, growth factors and cytokines that has been identified in the female reproductive tract from oocytes and granulosa cells of the ovary to uterine epithelial and stromal cells. In the present study we used transgenic...

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Autores principales: Robker, Rebecca L., Watson, Laura N., Robertson, Sarah A., Dunning, Kylie R., McLaughlin, Eileen A., Russell, Darryl L.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4077744/
https://www.ncbi.nlm.nih.gov/pubmed/24983622
http://dx.doi.org/10.1371/journal.pone.0101182
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author Robker, Rebecca L.
Watson, Laura N.
Robertson, Sarah A.
Dunning, Kylie R.
McLaughlin, Eileen A.
Russell, Darryl L.
author_facet Robker, Rebecca L.
Watson, Laura N.
Robertson, Sarah A.
Dunning, Kylie R.
McLaughlin, Eileen A.
Russell, Darryl L.
author_sort Robker, Rebecca L.
collection PubMed
description The STAT3 transcription factor is a pleiotropic transducer of signalling by hormones, growth factors and cytokines that has been identified in the female reproductive tract from oocytes and granulosa cells of the ovary to uterine epithelial and stromal cells. In the present study we used transgenic models to investigate the importance of STAT3 for reproductive performance in these different tissues. The Cre-LoxP system was used to delete STAT3 in oocytes by crossing Stat3(fl/fl) with Zp3-cre+ mice, or in ovarian granulosa cells and uterine stroma by crossing with Amhr2-Cre+ mice. Surprisingly, deletion of STAT3 in oocytes had no effect on fertility indicating that the abundance of STAT3 protein in maturing oocytes and fertilized zygotes is not essential to these developmental stages. In Stat3(fl/fl);Amhr2-cre+ females impaired fertility was observed through significantly fewer litters and smaller litter size. Ovulation rate, oocyte fertilization and development to blastocyst were unaffected in this line; however, poor recombination efficiency in granulosa cells had yielded no net change in STAT3 protein abundance. In contrast, uteri from these mice showed STAT3 protein depletion selectively from the stomal compartment. A significant reduction in number of viable fetuses on gestational day 18, increased fetal resorptions and disrupted placental morphology were evident causes of the reduced fertility. In conclusion, this study defines an important role for STAT3 in uterine stromal cells during embryo implantation and the development of a functional placenta.
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spelling pubmed-40777442014-07-03 Identification of Sites of STAT3 Action in the Female Reproductive Tract through Conditional Gene Deletion Robker, Rebecca L. Watson, Laura N. Robertson, Sarah A. Dunning, Kylie R. McLaughlin, Eileen A. Russell, Darryl L. PLoS One Research Article The STAT3 transcription factor is a pleiotropic transducer of signalling by hormones, growth factors and cytokines that has been identified in the female reproductive tract from oocytes and granulosa cells of the ovary to uterine epithelial and stromal cells. In the present study we used transgenic models to investigate the importance of STAT3 for reproductive performance in these different tissues. The Cre-LoxP system was used to delete STAT3 in oocytes by crossing Stat3(fl/fl) with Zp3-cre+ mice, or in ovarian granulosa cells and uterine stroma by crossing with Amhr2-Cre+ mice. Surprisingly, deletion of STAT3 in oocytes had no effect on fertility indicating that the abundance of STAT3 protein in maturing oocytes and fertilized zygotes is not essential to these developmental stages. In Stat3(fl/fl);Amhr2-cre+ females impaired fertility was observed through significantly fewer litters and smaller litter size. Ovulation rate, oocyte fertilization and development to blastocyst were unaffected in this line; however, poor recombination efficiency in granulosa cells had yielded no net change in STAT3 protein abundance. In contrast, uteri from these mice showed STAT3 protein depletion selectively from the stomal compartment. A significant reduction in number of viable fetuses on gestational day 18, increased fetal resorptions and disrupted placental morphology were evident causes of the reduced fertility. In conclusion, this study defines an important role for STAT3 in uterine stromal cells during embryo implantation and the development of a functional placenta. Public Library of Science 2014-07-01 /pmc/articles/PMC4077744/ /pubmed/24983622 http://dx.doi.org/10.1371/journal.pone.0101182 Text en © 2014 Robker et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Robker, Rebecca L.
Watson, Laura N.
Robertson, Sarah A.
Dunning, Kylie R.
McLaughlin, Eileen A.
Russell, Darryl L.
Identification of Sites of STAT3 Action in the Female Reproductive Tract through Conditional Gene Deletion
title Identification of Sites of STAT3 Action in the Female Reproductive Tract through Conditional Gene Deletion
title_full Identification of Sites of STAT3 Action in the Female Reproductive Tract through Conditional Gene Deletion
title_fullStr Identification of Sites of STAT3 Action in the Female Reproductive Tract through Conditional Gene Deletion
title_full_unstemmed Identification of Sites of STAT3 Action in the Female Reproductive Tract through Conditional Gene Deletion
title_short Identification of Sites of STAT3 Action in the Female Reproductive Tract through Conditional Gene Deletion
title_sort identification of sites of stat3 action in the female reproductive tract through conditional gene deletion
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4077744/
https://www.ncbi.nlm.nih.gov/pubmed/24983622
http://dx.doi.org/10.1371/journal.pone.0101182
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