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Title: Targeted ablation of gonadotrophs in transgenic mice depresses prolactin but not growth hormone gene expression at birth as measured by quantitative mRNA detection
Authors: Vankelecom, Hugo ×
Seuntjens, Eve
Hauspie, Annelies
Denef, Carl #
Issue Date: Nov-2003
Series Title: Journal of biomedical science. vol:10 issue:6 Pt 2 pages:805-12
Abstract: We previously reported that transgenic ablation of gonadotrophs results in impaired development of cells immunostainable for prolactin (PRL) but not of cells immunostainable for growth hormone (GH) or pro-opiomelanocortin (POMC) in pituitary of newborn mice. The question remained whether this reduction in PRL protein is a reflection of reduced PRL mRNA expression, or whether this regulation is only situated at the translational level. We therefore generated a new series of transgenic mice in which gonadotrophs were ablated by diphtheria toxin A targeting, and analyzed hormone mRNA levels instead of hormone protein around the day of birth. Pituitary mRNA expression levels of luteinizing hormone-beta (LHbeta), PRL and GH were quantified using real-time TaqMan RT-PCR. Of the 13 transgenic mice obtained, 8 showed a clear-cut reduction (ranging from 62 to 98%) in LHbeta mRNA levels. PRL mRNA values were significantly reduced in the transgenic mice (p = 0.0034), while GH mRNA expression was unaffected (p = 0.93). An additional observation was that female newborn mice produce 5 times more LHbeta mRNA than male mice whereas no sex difference was observed for expression levels of PRL and GH mRNA. Moreover, in the wild-type mice, LHbeta mRNA expression was 20-fold higher than GH mRNA expression which in turn was 500- to 1,000-fold higher than PRL mRNA expression, suggesting a low expression level of the PRL gene at birth. In conclusion, the present data support the hypothesis that embryonic development of PRL gene expression is stimulated by gonadotrophs.
URI: 
ISSN: 1021-7770
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Pharmacology Section (-)
Laboratory of Tissue Plasticity (-)
× corresponding author
# (joint) last author

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