| Use of a prolactin-Cre/ROSA-YFP transgenic mouse provides no evidence for lactotroph transdifferentiation after weaning, or increase in lactotroph/somatotroph proportion in lactation. | |
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MedLine Citation:
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PMID: 20139144 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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In rats, a shift from somatotroph dominance to lactotroph dominance during pregnancy and lactation is well reported. Somatotroph to lactotroph transdifferentiation and increased lactotroph mitotic activity are believed to account for this and associated pituitary hypertrophy. A combination of cell death and transdifferentiation away from the lactotroph phenotype has been reported to restore non-pregnant pituitary proportions after weaning. To attempt to confirm that a similar process occurs in mice, we generated and used a transgenic reporter mouse model (prolactin (PRL)-Cre/ROSA26-expression of yellow fluorescent protein (EYFP)) in which PRL promoter activity at any time resulted in permanent, stable, and highly specific EYFP. Triple immunochemistry for GH, PRL, and EYFP was used to quantify EYFP+ve, PRL-ve, and GH+ve cell populations during pregnancy and lactation, and for up to 3 weeks after weaning, and concurrent changes in cell size were estimated. At all stages, the EYFP reporter was expressed in 80% of the lactotrophs, but in fewer than 1% of other pituitary cell types, indicating that transdifferentiation from those lactotrophs where reporter expression was activated is extremely rare. Contrary to expectations, no increase in the lactotroph/somatotroph ratio was seen during pregnancy and lactation, whether assessed by immunochemistry for the reporter or PRL: findings confirmed by PRL immunochemistry in non-transgenic mice. Mammosomatotrophs were rarely encountered at the age group studied. Individual EYFP+ve cell volumes increased significantly by mid-lactation compared with virgin animals. This, in combination with a modest and non-cell type-specific estrogen-induced increase in mitotic activity, could account for pregnancy-induced changes in overall pituitary size. |
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Authors:
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Emma Castrique; Marta Fernandez-Fuente; Paul Le Tissier; Andy Herman; Andy Levy |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-02-05 |
Journal Detail:
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Title: The Journal of endocrinology Volume: 205 ISSN: 1479-6805 ISO Abbreviation: J. Endocrinol. Publication Date: 2010 Apr |
Date Detail:
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Created Date: 2010-03-15 Completed Date: 2010-04-08 Revised Date: 2011-04-28 |
Medline Journal Info:
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Nlm Unique ID: 0375363 Medline TA: J Endocrinol Country: England |
Other Details:
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Languages: eng Pagination: 49-60 Citation Subset: IM |
Affiliation:
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Henry Wellcome Labs for Integrative Neuroscience and Endocrinology, University of Bristol, Dorothy Hodgkin Building, Bristol, UK. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cell Death Cell Differentiation Female Growth Hormone / metabolism Integrases / genetics, metabolism* Lactation / metabolism* Lactotrophs / cytology, metabolism* Luminescent Proteins / genetics, metabolism Male Mice Mice, Inbred C57BL Mice, Inbred CBA Mice, Transgenic Models, Animal Phenotype Pregnancy Prolactin / genetics, metabolism* Proteins / genetics, metabolism* Somatotrophs / cytology, metabolism* Weaning |
| Grant Support | |
ID/Acronym/Agency:
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//Medical Research Council; //Wellcome Trust |
| Chemical | |
Reg. No./Substance:
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0/Gt(ROSA)26Sor protein, mouse; 0/Luminescent Proteins; 0/Proteins; 9002-62-4/Prolactin; 9002-72-6/Growth Hormone; EC 2.7.7.-/Cre recombinase; EC 2.7.7.-/Integrases |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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