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J Biol Chem, Vol. 275, Issue 15, 11404-11411, April 14, 2000
From the Departments of Obstetrics and Gynecology and
§ Internal Medicine II, Faculty of Medicine, Osaka
University, 2-2 Yamada-oka, Suita, Osaka 565-0871, Japan
Estrogen exerts a variety of effects not only on
female reproductive organs but also on nonreproductive organs,
including adipose tissue. Estrogen inhibits obesity triggered by
ovariectomy in rodents. We studied the mechanism underlying this
estrogen-dependent inhibition of obesity. Estrogen markedly
decreased the amounts of fat accumulation and lipoprotein lipase (LPL)
mRNA as well as triglyceride accumulation in genetically
manipulated 3T3-L1 adipocytes stably expressing the estrogen receptor
(ER). A pLPL(1980)-CAT construct, along with an ER expression vector,
was introduced into differentiated 3T3-L1 cells, and CAT activities
were determined. ER, mostly ligand-dependently, inhibited
the basal LPL promoter activity by 7-fold. We searched the LPL promoter
for an estrogen-responsive suppressive element by employing a set of
5'-deletion mutants of the pLPL-CAT reporter. Although there was no
classical estrogen response element, it was demonstrated that an
AP-1-like TGAATTC sequence located at (
Estrogen Suppresses Transcription of Lipoprotein Lipase Gene
EXISTENCE OF A UNIQUE ESTROGEN RESPONSE ELEMENT ON THE
LIPOPROTEIN LIPASE PROMOTER*
,
1856/1850) was responsible
for the suppression of the LPL gene transcription by estrogen. An
electrophoretic mobility shift assay probed with the TGAATTC sequence
demonstrated formation of a specific DNA-nuclear protein complex.
Interestingly, this complex was not affected by the addition of any
antibodies against ER, c-Jun, c-Fos, JunB, or JunD. Because this
TGAATTC element responded to phorbol ester and overexpression of
CREB-binding protein abrogated the suppressive effect of estrogen on
the LPL promoter, we conclude that a unique protein that is related to the AP-1 transcription factor families may be involved in the complex
that binds to the TGAATTC element.
*
This work was supported by grants from the Ministry of
Education of Japan.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: Dept. of Obstetrics
and Gynecology E5, Faculty of Medicine, Osaka University, 2-2 Yamada-oka, Suita, Osaka 565-0871, Japan. Tel.: 81-6-6879-3351; Fax:
81-6-6879-3359; E-mail: ynishio@gyne.med.osaka-u.ac.jp.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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