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This Article Accepted manuscript (PDF) All Versions of this Article: JOE-08-0377v1 199/3/435    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Mikhaylova, I. Articles by Voutilainen, R. Search for Related Content PubMed PubMed Citation Articles by Mikhaylova, I. Articles by Voutilainen, R.

I Mikhaylova, Department of Pediatrics, Kuopio University, Kuopio, Finland
T Jaaskelainen, Biomedicine/Medical Biochemistry, University of Kuopio, Kuopio, Finland
J Jaaskelainen, Department Pediatrics, Kuopio University, Kuopio, Finland
J Palvimo, Institute of Biomedicine/Medical Biochemistry, University of Kuopio, Kuopio, Finland
R Voutilainen, Kuopio, FI-70211, Finland

Correspondence: Raimo Voutilainen, Email: raimo.voutilainen{at}uku.fi

Abstract

Leukemia inhibitory factor (LIF) is a multiple function cytokine regulating the hypothalamo-pituitary-adrenal axis at the pituitary level. LIF and its receptor are expressed in the adrenal glands, suggesting their potential regulatory role also at the adrenal level. Our aim was to clarify the effects of LIF on adrenal steroidogenesis using cell culture conditions. NCI-H295R human adrenocortical cells were treated with LIF (0.01-100 ng/ml) for 3-48 h with or without 8-Br-cAMP (1 mM). LIF treatment augmented cortisol, dehydroepiandrosterone, dehydroepiandrosterone sulphate, androstenedione, and aldosterone production (up to 224, 211, 149, 229 and 170% of control, respectively, P<0.05 for all). It increased basal steroidogenic acute regulatory protein (StAR) and 17-hydroxylase/17,20-lyase (CYP17) mRNAs (up to 142 and 170% of control, respectively, P<0.05) and the respective proteins, but decreased 3β-hydroxysteroid dehydrogenase type 2 (3β-HSD2) mRNA (down to 72% of control, P<0.05) and protein. LIF also increased 8-Br-cAMP-induced cortisol and DHEA production and StAR mRNA accumulation, while it attenuated 8-Br-cAMP-induced 3β-HSD2 expression and androstenedione production. It had an additive effect on TNF--induced cortisol production. LIF had no effect on apoptosis, but it increased slightly the number of metabolically active cells (up to 120% of control, P<0.05). These findings indicate that LIF is a potential physiologic and/or pathophysiologic regulator of steroidogenesis at the adrenal level.

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