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.

摘要: In rats, a shift from somatotroph dominance to lactotroph during pregnancy and lactation is well reported. Somatotroph transdifferentiation increased mitotic activity are believed account for this associated pituitary hypertrophy. A combination of cell death away the phenotype has been reported restore non-pregnant proportions after weaning. To attempt confirm that similar process occurs in mice, we generated used transgenic reporter mouse model (prolactin (PRL)-Cre/ROSA26-expression yellow fluorescent protein (EYFP)) which PRL promoter at any time resulted permanent, stable, highly specific EYFP. Triple immunochemistry GH, PRL, EYFP was quantify EYFP+ve, PRL−ve, GH+ve populations lactation, up 3 weeks weaning, concurrent changes size were estimated. At all stages, expressed 80% lactotrophs, but fewer than 1% other types, indicating those lactotrophs where expression activated extremely rare. Contrary expectations, no increase lactotroph/somatotroph ratio seen whether assessed by or PRL: findings confirmed non-transgenic mice. Mammosomatotrophs rarely encountered age group studied. Individual EYFP+ve volumes significantly mid-lactation compared with virgin animals. This, modest non-cell type-specific estrogen-induced activity, could pregnancy-induced overall size.