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J. Biol. Chem., Vol. 275, Issue 26, 20204-20209, June 30, 2000
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From the Department of Cell Biology and Biochemistry, Texas Tech
University Health Sciences Center, Lubbock, Texas 79430
This study was conducted to examine the mechanism
for arachidonic acid (AA) regulation of steroidogenic acute regulatory
(StAR) protein expression and the relationship between AA and cAMP in hormone-induced steroidogenesis. Dibutyryl cyclic AMP
(Bt2cAMP)-stimulated MA-10 Leydig cells were treated
with AA and/or the phospholipase A2 inhibitor,
dexamethasone. Dexamethasone significantly reduced Bt2cAMP-stimulated progesterone production, StAR promoter
activity, StAR mRNA, and StAR protein. The inhibitory effects of
dexamethasone were reversed by the addition of 150 µM AA
to MA-10 cells. In addition, MA-10 cells were treated with the
lipoxygenase inhibitor, nordihydroguaiaretic acid (NDGA), the
5-lipoxygenase inhibitor, AA861, the epoxygenase inhibitor, miconazole,
and the cyclooxygenase inhibitor, indomethacin. Both NDGA and AA861
inhibited progesterone production and StAR protein expression.
AA861-inhibited progesterone synthesis and StAR protein were partially
reversed by addition of the 5- lipoxygenase metabolite,
5(S)-hydroperoxy-(6E,8Z,11Z,14Z)-eicosatetraenoic acid. Inhibition of epoxygenase activity inhibited progesterone production significantly, but StAR protein was only slightly reduced. Indomethacin enhanced StAR protein expression and significantly increased progesterone production. Inhibition of AA release or lipoxygenase activities did not affect protein kinase A activity, whereas inhibition of protein kinase A activity using H89 reduced Bt2cAMP-induced StAR protein. AA alone did not induce StAR
protein expression nor steroid production. These results demonstrate
the essential role of AA in steroid biosynthesis and StAR gene
transcription and suggest the possible involvement of the lipoxygenase
pathway in steroidogenesis. This study further indicates that AA and
cAMP transduce signals from trophic hormone receptors to the nucleus through two separate pathways and act to co-regulate steroid production and StAR gene expression and indicates that both pathways are required
for trophic hormone-stimulated steroidogenesis.
The Role of Arachidonic Acid in Steroidogenesis and Steroidogenic
Acute Regulatory (StAR) Gene and Protein Expression*
*
The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed. Tel.: 806-743-2505;
Fax: 806-743-2990; E-mail: Doug.Stocco@ttmc.ttuhsc.edu.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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