Lack of prolactin receptor signaling in mice results in lactotroph proliferation and prolactinomas by dopamine-dependent and -independent mechanisms
Kathryn G. Schuff, … , Sylvia L. Asa, Malcolm J. Low
Kathryn G. Schuff, … , Sylvia L. Asa, Malcolm J. Low
Published October 1, 2002
Citation Information: J Clin Invest. 2002;110(7):973-981. https://doi.org/10.1172/JCI15912.
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Article Genetics

Lack of prolactin receptor signaling in mice results in lactotroph proliferation and prolactinomas by dopamine-dependent and -independent mechanisms

Abstract

Research Article

Authors

Kathryn G. Schuff, Shane T. Hentges, Michele A. Kelly, Nadine Binart, Paul A. Kelly, P. Michael Iuvone, Sylvia L. Asa, Malcolm J. Low

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Effect of PRL treatment on lactotroph proliferation in primary pituitary...
Effect of PRL treatment on lactotroph proliferation in primary pituitary cultures. Primary cultures were treated with increasing concentrations of mPRL. The proliferative index was calculated as the percentage of cells demonstrating immunoreactivity for both PRL and BrdU relative to the total number of PRL-immunoreactive cells. (a) PRL treatment reduced the proliferative index by a maximum of 75% in pituitary cultures from wild-type female mice. (b) PRL treatment had no effect on the lactotroph proliferative index in cultures from Drd2–/– female mice. (c) PRL treatment reduced the proliferative index by a maximum of 73% in pituitary cultures from Drd2–/– male mice. P < 0.001 for ANOVA of main effect of PRL treatment for wild-type female and Drd2–/– male pituitary cultures. *P < 0.001 compared with control medium without recombinant PRL by Fisher post hoc test.