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Other Original Articles |
Departments of Physiology (S.-J.T., C.-C.L., H.-M.C.) and Obstetrics and Gynecology (M.-H.W.), and Institute of Molecular Medicine (H.S.S.), National Cheng Kung University Medical College, Tainan 70101, Taiwan, Republic of China
Address all correspondence and requests for reprints to: Shaw-Jenq Tsai, Ph.D., Department of Physiology, National Cheng Kung University Medical College, Tainan 701, Taiwan, Republic of China. E-mail: seantsai{at}mail.ncku.edu.tw
Abstract
The regulation of steroidogenic acute regulatory protein (StAR)
gene expression and the synthesis of steroids from cholesterol in
ectopic endometriosis tissues were investigated. Peritoneal fluid and
endometrial tissues were collected from patients with endometriosis and
otherwise healthy women. Peritoneal progesterone and 17ß-E2
concentrations were highest in early stage endometriosis compared with
those in advanced stage endometriosis and in normal women. In
concordance with the profile of peritoneal steroids, StAR mRNA and
protein were greatest in ectopic implants of early endometriosis. In
the advanced stage, concentrations of StAR mRNA and protein were also
greater compared with those in normal endometrium. In contrast, P450
side-chain cleavage enzyme and 3ß-hydroxysteroid dehydrogenase
transcripts were not different between normal endometrium and ectopic
endometriotic implants. Expression of StAR mRNA was detected in
purified stromal, but not epithelial, cells. Treatment with
PGE2, but not TNF
, or IL-1ß significantly increased
StAR expression and thus induced progesterone production in cultured
endometriotic stromal cells. These results demonstrated that aberrant
expression of StAR in ectopic endometriotic tissues leading to
increased peritoneal progesterone is associated with the formation of
endometriosis. Induction of StAR gene expression by peritoneal
PGE2 in endometriotic stromal cells may further contribute
to the development of endometriosis.
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