Tenascin is highly expressed in endometriosis and its expression is upregulated by estrogen.
OBJECTIVE
To investigate the localization of tenascin expression in the endometrium of women without endometriosis and in endometriotic implants, and to determine the in vitro regulation of tenascin by E(2) in these tissues.


METHODS
Experimental laboratory study.


METHODS
University medical center.


METHODS
Reproductive age women with or without endometriosis.


METHODS
Proliferative (n = 14), and secretory (n = 14) endometrium from women without endometriosis and endometriosis implants (n = 14) were used for immunohistochemical analysis. Endometrial and endometriotic stromal cells were grown in culture and treated with E(2), the estrogen receptor antagonist ICI 182 780 (ICI) alone, E(2) in combination with ICI, or vehicle (control) for 24 hours, and tenascin expression was analyzed by Western blotting.


METHODS
Expression levels of tenascin in normal endometrium and endometriotic implants and its regulation by E(2).


RESULTS
Tenascin immunostaining revealed an increasing intensity in the stromal cells, starting from normal secretory endometrium, then normal proliferative endometrium, and reaching the highest expression in endometriotic implants. Estradiol induced a significant increase in tenascin protein levels in the endometriotic stromal cells in culture.


CONCLUSIONS
The modulation of tenascin as an extracellular matrix protein by E(2) in endometriotic stromal cells may be one of the factors playing a role in the development of endometriosis.
Tan
Orkun
O
Division of Reproductive Endocrinology and Infertility, Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, Connecticut; Department of Obstetrics and Gynecology, Bridgeport Hospital, Bridgeport, Connecticut.
Ornek
Turkan
T
Division of Reproductive Endocrinology and Infertility, Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, Connecticut; Department of Obstetrics and Gynecology, Ufuk University School of Medicine, Ankara, Turkey.
Seval
Yasemin
Y
Division of Reproductive Endocrinology and Infertility, Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, Connecticut; Department of Histology and Embryology Faculty of Medicine, Akdeniz University, Antalya, Turkey.
Sati
Leyla
L
Division of Reproductive Endocrinology and Infertility, Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, Connecticut; Department of Histology and Embryology Faculty of Medicine, Akdeniz University, Antalya, Turkey.
Arici
Aydin
A
Division of Reproductive Endocrinology and Infertility, Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, Connecticut. Electronic address: aydin.arici@yale.edu.
D000328:Adult; D049109:Cell Proliferation; D002478:Cells, Cultured; D004715:Endometriosis / Q000378:metabolism* / Q000473:pathology; D004717:Endometrium / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D004958:Estradiol / Q000031:analogs & derivatives / Q000494:pharmacology / Q000502:physiology*; D004965:Estrogen Antagonists / Q000494:pharmacology; D004967:Estrogens / Q000502:physiology*; D005109:Extracellular Matrix / Q000378:metabolism; D005260:Female; D000077267:Fulvestrant; D006801:Humans; D008875:Middle Aged; D019063:Tenascin / Q000235:genetics / Q000378:metabolism*; D015854:Up-Regulation / Q000187:drug effects*
D004965:Estrogen Antagonists; D004967:Estrogens; D019063:Tenascin; D000077267:Fulvestrant; D004958:Estradiol