Decidualization attenuates the contractility of eutopic and ectopic endometrial stromal cells: implications for hormone therapy of endometriosis.
BACKGROUND
Decidualization of the endometrium involves the morphological and biochemical reprogramming of the estrogen-primed proliferative endometrial stromal compartment under the continuing influence of progesterone.


OBJECTIVE
The aim of this study was to evaluate the involvement of the extracellular matrix contractility of eutopic and ectopic endometrial stromal cells during the tissue remodeling processes associated with decidualization.


METHODS
The effect of decidualization on the contractile profile of the endometriotic cyst stromal cells and eutopic endometrial stromal cells with or without endometriosis in the three-dimensional collagen gel culture was investigated using laser scanning microscopy, collagen gel contraction assays, and Western blot analysis.


RESULTS
Decidualized ectopic and eutopic endometrial stromal cells in the three-dimensional collagen gel culture mimicked the morphology of decidual tissue in vivo. In vitro decidualization inhibited the contractility of these eutopic and ectopic endometrial stromal cells. Down-regulation of integrin alpha1beta1 and alpha2beta1 expression, suppression of Ras homology A (Rho A), Rho-associated coiled-coil-forming protein kinase (ROCK)-I and ROCK-II expression, inhibition of the differentiation into the myofibroblastic phenotype, and induction of differentiation into epithelioid decidual phenotype were observed in these cells during decidualization.


CONCLUSIONS
It is suggested that the attenuation of eutopic endometrial stromal cell-mediated contractility by decidualization is a novel and integral mechanism of the physiological endometrial tissue remodeling process during menstrual cycles. Although ectopic endometrial stromal cells have enhanced contractile profile, decidualization can attenuate the contractility of these cells. These findings may be one of the action mechanisms by which oral contraceptives and progestins ameliorate endometriosis.
Department of Obstetrics and Gynecology, Faculty of Medicine, Oita University, Idaigaoka 1-1, Hasama-machi, Yufu-shi, Oita 879-5593, Japan.
Akitoshi
A
Tsuno
Kaei
K
Nasu
Akitoshi
A
Yuge
Harunobu
H
Matsumoto
Masakazu
M
Nishida
Hisashi
H
Narahara
D000328:Adult; D003994:Bucladesine / Q000008:administration & dosage; D002465:Cell Movement / Q000187:drug effects / Q000502:physiology; D002478:Cells, Cultured; D002828:Choristoma / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology; D003656:Decidua / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology / Q000502:physiology*; D004715:Endometriosis / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology*; D004717:Endometrium / Q000187:drug effects / Q000378:metabolism / Q000473:pathology / Q000502:physiology*; D005260:Female; D006728:Hormones / Q000494:pharmacology* / Q000627:therapeutic use; D006801:Humans; D018970:Insulin-Like Growth Factor Binding Protein 1 / Q000378:metabolism; D011372:Progestins / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use; D011388:Prolactin / Q000378:metabolism; D017154:Stromal Cells / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D014591:Uterine Diseases / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology*; D055815:Young Adult
D006728:Hormones; C032231:IGFBP1 protein, human; D018970:Insulin-Like Growth Factor Binding Protein 1; D011372:Progestins; D003994:Bucladesine; D011388:Prolactin