Title: Targeted ablation of gonadotrophs in transgenic mice affects embryonic development of lactotrophs
Authors: Seuntjens, Eve ×
Vankelecom, Hugo
Quaegebeur, Annelies
Vande Vijver, Veerle
Denef, Carl #
Issue Date: Sep-1999
Series Title: Molecular and cellular endocrinology. vol:150 issue:1-2 pages:129-139
Abstract: Ablation of pituitary gonadotrophs was obtained in transgenic mice expressing diphtheria toxin A (DTA) under control of the -313/+48 bovine glycoprotein hormone alpha-subunit (alphaSU) promoter, previously shown to be active in mouse gonadotrophs but not in thyrotrophs. Development of hormone-producing cell types was assessed on the day of birth by computer-assisted image analysis on paraffin-embedded, immunostained pituitary sections. Six out of 50 transgenic F0 ('founder') mice (3 males and 3 females) showed a nearly complete disappearance of gonadotrophs but not of thyrotrophs. The number of lactotrophs and the relative area occupied by PRL-immunoreactivity were significantly reduced in the gonadotroph-depleted mice. The size of lactotroph clusters was smaller in the absence of gonadotrophs. The number and immunoreactive area of corticotrophs and somatotrophs, on the other hand, were not significantly affected by gonadotroph ablation. Based on the reported evidence that fetal ovaries do not produce steroid hormones as a result of lack of expression of at least three of the steroidogenic enzymes, P450scc, P450c17, and P450arom, the present observations can hardly be explained by a decline in estrogen levels due to gonadotroph ablation. Rather, the present data indicate that gonadotrophs directly stimulate the development of lactotrophs during fetal and early postnatal life, consistent with previous in vitro observations, and/or that gonadotrophs may share a cell-lineage relationship with a subpopulation of lactotrophs.
ISSN: 0303-7207
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Pharmacology Section (-)
Laboratory of Tissue Plasticity (-)
Embryo and Stemcells (-)
× corresponding author
# (joint) last author

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