Endometrial Stromal Cells (endometrial + stromal_cell)

Distribution by Scientific Domains


Selected Abstracts


SHORT COMMUNICATION: Increased Expression of Glutathione by Estradiol, Tumor Necrosis Factor-Alpha, and Interleukin 1-Beta in Endometrial Stromal Cells

AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 6 2009
Sa Ra Lee
Problem, The intracellular antioxidant system, based on glutathione (GSH), plays a key role in endometrial detoxification reactions and has been proposed to be involved in the pathogenesis endometriosis. This study was designed to evaluate whether estradiol (E2) and proinflammatory cytokines have any effects on expression of glutathione in endometrial stromal cells (ESCs). Method of study, Glutathione levels were measured utilizing high-performance liquid chromatography following in vitro culture and treatment of ESCs with estradiol, tumor necrosis factor-alpha (TNF-,) and interleukin 1-beta (IL-1,). Results, The GSH level in E2 (10,8 m) treatment group was significantly higher than in the control group at 48 h (P < 0.05). In vitro treatment of ESCs with TNF-, 10 ng/mL as well as E2 (10,8 m) plus TNF-, 10 ng/mL for 48 hr also led to a significant increase in GSH level (P < 0.05; P < 0.05, respectively). Both IL-1, 10 ng/mL and E2 (10,8 m) plus IL-1, 10 ng/mL for 48 hr increased GSH level significantly (P < 0.05; P < 0.05, respectively) as well. Conclusions, These findings might suggest that increased production of estradiol and proinflammatory cytokines in the peritoneal cavity possibly leads to the establishment of endometriosis through increased level of GSH. [source]


Atrazine-induced changes in aromatase activity in estrogen sensitive target tissues

JOURNAL OF APPLIED TOXICOLOGY, Issue 3 2008
A. C. Holloway
Abstract Atrazine (ATR) is a pesticide used widely throughout North America. Although not directly estrogenic, ATR treatment has been shown to increase aromatase activity in tumor cell lines. Thus, it is suggested that ATR can increase local tissue estrogen levels in estrogen sensitive target tissues through increased aromatase activity. Therefore the effect of ATR on aromatase activity was measured in human granulosa-lutein cell cultures, cells that abundantly express aromatase, and endometrial stromal cell (ESC) cultures, cells that do not express aromatase. Aromatase activity was quantified by the tritiated water method and the specificity of the assay was confirmed by co-incubation with 4-hydroxyandrostenedione, an irreversible inhibitor of the catalytic activity of aromatase. Aromatase activity in ATR treated (1,10 µm) granulosa-lutein cells was increased more than 2-fold compared with control cultures. There were no treatment related changes in cellular protein and thus it is suggested that the ATR-induced change in aromatase activity was not due to an increase in cell number. ATR-treatment had no effect on ESC aromatase activity at any concentration tested. Similarly, there was no effect of ATR treatment on human recombinant aromatase activity in our cell-free test system. Therefore it is concluded that µm concentrations of ATR can increase aromatase activity of human granulosa cells but not ESC and this effect is not elicited at the enzyme level. Copyright © 2007 John Wiley & Sons, Ltd. [source]


Expression of nidogens in rat uterus and embryo during decidualization and implantation

JOURNAL OF MORPHOLOGY, Issue 7 2006
Hakan Öner
Abstract The purpose of this study was to demonstrate the expression of nidogen-1 and nidogen-2 and their possible role in decidualization and implantation events during early pregnancy in rats. The tissue samples were examined from pregnant animals between gestational days 1,8 using immunocytochemistry. The uterine luminal epithelium, the glandular epithelium, and the myometrial smooth muscle cells stained strongly from gestational days 1,8 with both nidogen antibodies. At day 4 the decidual reaction areas began to appear in the stromal matrix and immunostaining of both nidogens revealed that the basement membrane of the surface epithelium was discontinuous. The differentiation of stromal cells into decidual cells was seen at gestational day 5 and both nidogens were weakly expressed in the decidualizing cells. At day 6, nidogen-2 immunoreactivity was higher in the primary decidual cells close to the embryo than nidogen-1, and during development of the decidual tissue both nidogens appeared in the endometrial stromal cells. At day 7, while expression of both nidogens declined in the primary decidual cells, their expression was markedly observed in the secondary decidual cells close to the myometrium. At day 8, expression of both nidogens was also observed to increase in the primary decidual cells. While nidogen-2 expression was seen in the parietal endoderm and primary ectoderm of the rat embryos at this developmental stage, nidogen-1 expression was only detected in the parietal endoderm. These results indicate that nidogen-1 and nidogen-2 could play important roles during embryogenesis, decidualization, and implantation in the endometrium of rat uterus. J. Morphol. © 2006 Wiley-Liss, Inc. [source]


Adenomyosis with a sex cord-like stromal element

PATHOLOGY INTERNATIONAL, Issue 4 2000
Masaharu Fukunaga
A case of adenomyosis with a sex cord-like stromal element is described. The element was an incidental, solitary, microscopic finding in a focus of adenomyosis. It was characterized by cord and trabecular arrangements of round to polygonal shaped cells in the endometrioid stroma. The cells were immunohistochemically positive for desmin and alpha-smooth muscle actin but negative for sex cord markers (alpha-inhibin and O13). The element appears to originate from the endometrial stromal cells through smooth muscle metaplasia. [source]


SHORT COMMUNICATION: Increased Expression of Glutathione by Estradiol, Tumor Necrosis Factor-Alpha, and Interleukin 1-Beta in Endometrial Stromal Cells

AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 6 2009
Sa Ra Lee
Problem, The intracellular antioxidant system, based on glutathione (GSH), plays a key role in endometrial detoxification reactions and has been proposed to be involved in the pathogenesis endometriosis. This study was designed to evaluate whether estradiol (E2) and proinflammatory cytokines have any effects on expression of glutathione in endometrial stromal cells (ESCs). Method of study, Glutathione levels were measured utilizing high-performance liquid chromatography following in vitro culture and treatment of ESCs with estradiol, tumor necrosis factor-alpha (TNF-,) and interleukin 1-beta (IL-1,). Results, The GSH level in E2 (10,8 m) treatment group was significantly higher than in the control group at 48 h (P < 0.05). In vitro treatment of ESCs with TNF-, 10 ng/mL as well as E2 (10,8 m) plus TNF-, 10 ng/mL for 48 hr also led to a significant increase in GSH level (P < 0.05; P < 0.05, respectively). Both IL-1, 10 ng/mL and E2 (10,8 m) plus IL-1, 10 ng/mL for 48 hr increased GSH level significantly (P < 0.05; P < 0.05, respectively) as well. Conclusions, These findings might suggest that increased production of estradiol and proinflammatory cytokines in the peritoneal cavity possibly leads to the establishment of endometriosis through increased level of GSH. [source]


ORIGINAL ARTICLE: TNF, Gene Silencing Reduced Lipopolysaccharide-Promoted Proliferation of Endometriotic Stromal Cells

AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 4 2009
Ayako Miyamoto
Problem, We previously reported that lipopolysaccharide (LPS)-promoted endometriotic stromal cell (ESC) proliferation by inducing TNF, production. The aim of this study was to investigate the efficacy of TNF, gene silencing on LPS-treated ESCs. Method of study, Endometriotic stromal cells (ESCs) and endometrial stromal cells (ESCs) (EMSCs) were obtained from ovarian chocolate cysts and uterine myoma, respectively. Using PCR array, LPS-induced gene expression profiling after transfection of TNF, siRNA into ESCs was performed. Down-regulated genes by TNF, silencing were examined using real-time RT-PCR. Effect of TNF, silencing was examined using ELISA and BrdU incorporation, respectively. Results, In PCR array, TNF, silencing in ESCs repressed LPS-induced expression of cIAP2 and IL-8, NF,B pathway responsive genes. After adding LPS, the levels of cIAP2 and IL-8 expression in ESCs were higher compared with those in EMSCs. TNF, silencing attenuated the LPS-induced ESC proliferation. Conclusion, Tumor necrosis factor , may be involved in cell proliferation of endometriotic tissues. [source]


Alveolar soft part sarcoma of the endometrium with expression of CD10 and hormone receptors,

APMIS, Issue 7 2007
Case Report
Alveolar soft part sarcoma (ASPS) is a rare tumor of uncertain histogenesis, mainly localized in the extremities. ASPS originating in the uterine corpus is quite rare; only eight such cases have been reported in the literature. We here present another case of ASPS found in the endometrium in a 50-year-old woman. Metastatic malignant tumor, including ASPS from other organs, was excluded by physical examination and imaging modalities. Thallium 201 was only localized in the uterus. The tumor showed characteristic histological features of ASPS: alveolar architecture with fibrovascular septa and abundant eosinophilic granular cytoplasm with periodic acid-Schiff-positive crystalline material. Diffuse nuclear immunoreactivity for TFE3, a marker recently reported to be specific for ASPS, further supported the diagnosis of ASPS. Interestingly, this tumor was negative for myogenic markers, but positive for CD10, progesterone receptor, and estrogen receptor. These immunohistochemical results and the tumor location suggest a possible link between endometrial stromal cells and the development of this tumor. [source]


The role of activins during decidualisation of human endometrium

AUSTRALIAN AND NEW ZEALAND JOURNAL OF OBSTETRICS AND GYNAECOLOGY, Issue 3 2006
Rebecca L. JONES
Decidualisation of the endometrial stroma is critical to create a specialised environment for embryo implantation and trophoblast invasion; however, the mechanisms involved are poorly understood. We have established that activin A is an important regulator of decidualisation of endometrial stromal cells in vitro. Here we describe studies that verify the physiological significance of these findings. We demonstrate that high concentrations of activin A are produced by decidualising cells in excess of the antagonists, inhibin and follistatin, thus confirming its bioavailability within the decidual environment. Furthermore, we demonstrate that all components of the activin signalling pathway (activin receptors and Smads) are expressed in decidualised cells, and identify a downstream mechanism for activin in the endometrium, through the regulation of matrix metalloproteinases (MMPs). This new knowledge is important for understanding the roles for activins and inhibins in regulating fertility. [source]