title: Possible involvement of CD10 in the development of endometriosis due to its inhibitory effects on CD44-dependent cell adhesion.
abstract: A reduced response to progesterone in the eutopic endometrium with endometriosis and in endometriotic tissues is considered to be the underlying factor for endometriosis. CD10 is known to be expressed by endometrial and endometriotic stromal cells and may be induced by progestins, although the function of CD10 is not fully revealed in endometrial or endometriotic tissues. In the current study, the expression of CD10 was significantly increased by treatment of the cells with progesterone, 17β-estradiol, and dibutyryl cyclic adenosine monophosphate (cAMP) in the endometrial stromal cells. On the other hand, the expression of CD10 following treatment with progesterone, 17β-estradiol, and dibutyryl cAMP was not significantly increased in endometriotic stromal cells. The adhesion assay for endometrial and endometriotic stromal cells to hyaluronan using 5- or 6-(N-succinimidyloxycarbonyl)-fluorescein 3', 6'-diacetate-labeled cells demonstrated that the CD44-dependent adhesion of stromal cells was inhibited by CD10. As far as the induction of CD10 is concerned, the effect of progesterone was different between endometrial stromal cells and endometriotic stromal cells. CD10 might be involved in the development of endometriosis due to its influence on CD44-dependent cell adhesion.
authors: 1Department of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
authors: Akira
authors: A
authors: Iwase
authors: Tomomi
authors: T
authors: Kotani
authors: Maki
authors: M
authors: Goto
authors: Hiroharu
authors: H
authors: Kobayashi
authors: Sachiko
authors: S
authors: Takikawa
authors: Tatsuo
authors: T
authors: Nakahara
authors: Tomoko
authors: T
authors: Nakamura
authors: Mika
authors: M
authors: Kondo
authors: Bayasula
authors: Yoshinari
authors: Y
authors: Nagatomo
authors: Fumitaka
authors: F
authors: Kikkawa
mesh_terms: D003994:Bucladesine / Q000494:pharmacology; D002448:Cell Adhesion / Q000187:drug effects; D002478:Cells, Cultured; D004715:Endometriosis / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D004717:Endometrium / Q000187:drug effects / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D004958:Estradiol / Q000494:pharmacology; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D018960:Hyaluronan Receptors / Q000378:metabolism*; D006820:Hyaluronic Acid / Q000378:metabolism; D015260:Neprilysin / Q000235:genetics / Q000378:metabolism*; D061251:Primary Cell Culture; D011374:Progesterone / Q000494:pharmacology; D011388:Prolactin / Q000378:metabolism; D034622:RNA Interference; D017154:Stromal Cells / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D013997:Time Factors; D014162:Transfection
chemical_list: C497483:CD44 protein, human; D018960:Hyaluronan Receptors; D011374:Progesterone; D004958:Estradiol; D003994:Bucladesine; D011388:Prolactin; D006820:Hyaluronic Acid; D015260:Neprilysin
keywords: CD10; CD44; adhesion; endometriosis; stromal cells.
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