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Department of Physiology, Institute of Biomedicine, University of Turku, Kiinamyllynkatu 10, FIN-20520 Turku, Finland
Address all correspondence and requests for reprints to: Ilpo T. Huhtaniemi, M.D., Ph.D., Department of Physiology, University of Turku, FIN-20520 Turku, Finland. E-mail: ilpo.huhtaniemi{at}utu.fi
We investigated in this study the effects of ovine PRL on endocrine
functions of cultured murine Leydig tumor cells (mLTC-1). The
parameters studied were the activation of signal transduction systems
involving cAMP and intracellular free Ca2+, the expression
of Janus kinase 2 (JAK2), expression and function of LH and PRL
receptors (R), expression of the steroidogenic acute regulatory (StAR)
protein, and stimulation of steroidogenesis. Very similar biphasic
dose- and time-dependent responses of all the parameters studied were
found upon PRL stimulation, comprising a fast inhibition within 24
h in response to high PRL doses (
30 µg/liter), and a slow
stimulation, between 48–72 h, in response to lower PRL doses (1–10
µg/liter). In addition, extracellular Ca2+ (1.5
mmol/liter) increased the effect of PRL on human CG (hCG)-stimulated
StAR messenger RNA expression and progesterone (P) production.
Importantly, the biphasic effects of PRL on LHR gene expression and
hCG-mediated P production were abolished in the presence of anti-PRL
antiserum, demonstrating specificity of PRL action. The PRL effects on
StAR expression, and steroid and cAMP production, apparently reflect
its effects on LHR function. The relevance of the PRL effects observed
in mLTC-1 cells was supported by demonstration of similar PRL responses
in hCG-stimulated testosterone production of isolated mouse Leydig
cells. Collectively, these findings clearly demonstrate the biphasic
regulatory actions of PRL, and clarify some facets of the controversial
role of this hormone in Leydig cell function.
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