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      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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          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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          Most cited references33

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          Vagaries of conditional gene targeting.

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            Pituitary gland growth during normal pregnancy: an in vivo study using magnetic resonance imaging.

            Autopsy studies have shown that pregnancy results in physiologic pituitary enlargement. We used magnetic resonance imaging (MRI) to corroborate those findings in vivo. Based on gestational age, 32 normal primigravid patients were divided into three groups: Group I (n = 10), less than 12 gestational weeks; Group II (n = 11), 13 to 26 gestational weeks; and Group III (n = 11), 27 gestational weeks or more. The pituitary dimensions and volumes in these groups were compared with those in 20 healthy nulliparous women (control group). MRI measurements showed a significant increase in pituitary volume in Groups I, II, and III when compared with the control group (p less than 0.001). Furthermore, there was an increase in pituitary volume between Groups I and II and between Groups II and III, although the former was not statistically significant (p greater than 0.05). At the end of pregnancy, the hypophysis had increased 2.6 mm in vertical, anteroposterior, and transversal dimensions, with an overall increase of 136 percent when compared with that of the control group. Baseline measurements of the normal enlargement of the pituitary gland that occurs during pregnancy could prove useful when evaluating pregnant patients with suspected pituitary tumors or lymphocytic hypophysitis.
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              Size and shape of the pituitary gland during pregnancy and post partum: measurement with MR imaging.

              Cranial magnetic resonance (MR) imaging was performed in 38 pregnant and postpartum women and 30 nonpregnant age-matched control subjects to establish standards for pituitary gland size and shape during this period. Gland height and infundibulum width were measured on midline T1-weighted sagittal images. Gland convexity or concavity was graded qualitatively. Throughout pregnancy, gland height increased linearly by approximately 0.08 mm/wk. No gland exceeded 10 mm in height during pregnancy. Increases in gland convexity also correlated with progression of pregnancy. The largest glands were seen in the immediate postpartum period; during this period, five of 12 glands measured 10.0-11.8 mm. Beyond the first week post partum, glands rapidly returned to normal size, apparently regardless of the status of breast-feeding. The mean diameter of the infundibulum was 2.2 mm (range, 0.8-4.0 mm). The pituitary gland enlarges throughout pregnancy but should probably not exceed 10 mm during most of this period. Size of up to 12 mm may be acceptable immediately post partum.

                Author and article information

                J Endocrinol
                The Journal of Endocrinology
                BioScientifica (Bristol )
                April 2010
                5 February 2010
                : 205
                : 1
                : 49-60
                [1 ]simpleHenry Wellcome Labs for Integrative Neuroscience and Endocrinology simpleUniversity of Bristol Dorothy Hodgkin Building, Whitson Street, Bristol, BS1 3NYUK
                [2 ]simpleDivision of Molecular Neuroendocrinology simpleNational Institute for Medical Research The Ridgeway, Mill Hill, , London, NW7 1AAUK
                [3 ]simpleDepartment of Cellular and Molecular Medicine, School of Medical Sciences simpleUniversity Walk Clifton, BristolUK
                Author notes
                (Correspondence should be addressed to A Levy who is now at Bristol University and United Bristol Healthcare Trust, Bristol, UK; Email: a.levy@ 123456bris.ac.uk )
                © 2010 Society for Endocrinology

                This is an Open Access article distributed under the terms of the Society for Endocrinology's Re-use Licence which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                : 29 January 2010
                : 5 February 2010
                Funded by: Wellcome Trust
                Funded by: Medical Research Council
                Regular Papers

                Endocrinology & Diabetes
                Endocrinology & Diabetes


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