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A Prolactin Family Paralog Regulates Placental Adaptations to a Physiological Stressor
The prolactin (PRL) family of hormones and cytokines participates in the regulation of optimal reproductive performance in the mouse and rat. Members of the PRL family are expressed in the anterior pituitary, uterus, and/or placenta. In the present study, we investigated the ontogeny of PRL family 7...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Society for the Study of Reproduction, Inc.
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4939737/ https://www.ncbi.nlm.nih.gov/pubmed/26985002 http://dx.doi.org/10.1095/biolreprod.115.138032 |
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author | Bu, Pengli Alam, Sheikh M. Khorshed Dhakal, Pramod Vivian, Jay L. Soares, Michael J. |
author_facet | Bu, Pengli Alam, Sheikh M. Khorshed Dhakal, Pramod Vivian, Jay L. Soares, Michael J. |
author_sort | Bu, Pengli |
collection | PubMed |
description | The prolactin (PRL) family of hormones and cytokines participates in the regulation of optimal reproductive performance in the mouse and rat. Members of the PRL family are expressed in the anterior pituitary, uterus, and/or placenta. In the present study, we investigated the ontogeny of PRL family 7, subfamily b, member 1 (PRL7B1; also called PRL-like protein-N, PLP-N) expression in the developing mouse placenta and established a mouse model for investigating the biological function of PRL7B1. Transcripts for Prl7b1 were first detected on Gestation Day (d) 8.5. From gestation d8.5 through d14.5, Prl7b1 was expressed in trophoblast cells residing at the interface between maternal mesometrial decidua and the developing placenta. On gestation d17.5, the predominant cellular source of Prl7b1 mRNA was migratory trophoblast cells invading into the uterine mesometrial decidua. The Prl7b1 null mutant allele was generated via replacement of the endogenous Prl7b1 coding sequence with beta-galactosidase (LacZ) reporter and neomycin cassettes. The mutant Prl7b1 allele was successfully passed through the germline. Homozygous Prl7b1 mutant mice were viable and fertile. Under standard animal housing conditions, Prl7b1 had undetectable effects on placentation and pregnancy. Hypoxia exposure during pregnancy evoked adaptations in the organization of the wild-type placenta that were not observed in Prl7b1 null placentation sites. In summary, PRL7B1 is viewed as a part of a pathway regulating placental adaptations to physiological stressors. |
format | Online Article Text |
id | pubmed-4939737 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Society for the Study of Reproduction, Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-49397372017-05-01 A Prolactin Family Paralog Regulates Placental Adaptations to a Physiological Stressor Bu, Pengli Alam, Sheikh M. Khorshed Dhakal, Pramod Vivian, Jay L. Soares, Michael J. Biol Reprod Articles The prolactin (PRL) family of hormones and cytokines participates in the regulation of optimal reproductive performance in the mouse and rat. Members of the PRL family are expressed in the anterior pituitary, uterus, and/or placenta. In the present study, we investigated the ontogeny of PRL family 7, subfamily b, member 1 (PRL7B1; also called PRL-like protein-N, PLP-N) expression in the developing mouse placenta and established a mouse model for investigating the biological function of PRL7B1. Transcripts for Prl7b1 were first detected on Gestation Day (d) 8.5. From gestation d8.5 through d14.5, Prl7b1 was expressed in trophoblast cells residing at the interface between maternal mesometrial decidua and the developing placenta. On gestation d17.5, the predominant cellular source of Prl7b1 mRNA was migratory trophoblast cells invading into the uterine mesometrial decidua. The Prl7b1 null mutant allele was generated via replacement of the endogenous Prl7b1 coding sequence with beta-galactosidase (LacZ) reporter and neomycin cassettes. The mutant Prl7b1 allele was successfully passed through the germline. Homozygous Prl7b1 mutant mice were viable and fertile. Under standard animal housing conditions, Prl7b1 had undetectable effects on placentation and pregnancy. Hypoxia exposure during pregnancy evoked adaptations in the organization of the wild-type placenta that were not observed in Prl7b1 null placentation sites. In summary, PRL7B1 is viewed as a part of a pathway regulating placental adaptations to physiological stressors. Society for the Study of Reproduction, Inc. 2016-03-16 2016-05 /pmc/articles/PMC4939737/ /pubmed/26985002 http://dx.doi.org/10.1095/biolreprod.115.138032 Text en © 2016 by the Society for the Study of Reproduction, Inc. http://creativecommons.org/licenses/by-nc/4.0/ This article is available under a Creative Commons License 4.0 (Attribution-Non-Commercial), as described at http://creativecommons.org/licenses/by-nc/4.0 |
spellingShingle | Articles Bu, Pengli Alam, Sheikh M. Khorshed Dhakal, Pramod Vivian, Jay L. Soares, Michael J. A Prolactin Family Paralog Regulates Placental Adaptations to a Physiological Stressor |
title | A Prolactin Family Paralog Regulates Placental Adaptations to a Physiological Stressor |
title_full | A Prolactin Family Paralog Regulates Placental Adaptations to a Physiological Stressor |
title_fullStr | A Prolactin Family Paralog Regulates Placental Adaptations to a Physiological Stressor |
title_full_unstemmed | A Prolactin Family Paralog Regulates Placental Adaptations to a Physiological Stressor |
title_short | A Prolactin Family Paralog Regulates Placental Adaptations to a Physiological Stressor |
title_sort | prolactin family paralog regulates placental adaptations to a physiological stressor |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4939737/ https://www.ncbi.nlm.nih.gov/pubmed/26985002 http://dx.doi.org/10.1095/biolreprod.115.138032 |
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