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Department of Medicine Cedars-Sinai Research Institute University of California Los Angeles School of Medicine Los Angeles, California 90048
Leukemia inhibitory factor (LIF) regulates the
mature hypothalamic-pituitary-adrenal axis in vivo.
In vitro, LIF determines corticotroph cell proliferation
and induces POMC transcription. To explore LIF action on pituitary
development, transgenic mice expressing LIF driven by the pituitary
glycoprotein hormone 
-subunit (GSU) promoter were generated.
Transgenic mice exhibited dwarfism with low IGF-I (29 ± 9 ng/ml
vs. wild type (WT) 137 ± 16 ng/ml; P
< 0.001), hypogonadism with low FSH (0.04 ± 0.023 ng/ml
vs. WT 0.63 ± 0.18 ng/ml; P <
0.001), and Cushingoid features of thin skin and truncal obesity with
elevated cortisol levels (86 ± 22 ng/ml vs. WT
50 ± 14 ng/ml; P = 0.002). Their pituitary
glands showed corticotroph hyperplasia, striking somatotroph and
gonadotroph hypoplasia, and multiple Rathke-like cysts lined by
ciliated cells. LIF, overexpressed in Rathke’s pouch at embryonal day
10, diverts the differentiation stream of hormone-secreting cells
toward the corticotroph lineage and ciliated nasopharyngeal-like
epithelium. Thus, inappropriate expression of LIF, a neuro-immune
interfacing cytokine, plays a key role in the terminal differentiation
events of pituitary development and mature pituitary function.
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