FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2055069536> ?p ?o ?g. }

• W2055069536 endingPage "1838" @default.
• W2055069536 startingPage "1836" @default.
• W2055069536 abstract "Cell proliferation of endometrial stromal cells treated with peritoneal fluid of women (aged 25 to 43 years) with endometriosis (n = 12) statistically significantly increased compared with the control treatment (peritoneal fluid of women without endometriosis, n = 8). Also, COX-2 gene expression and prostaglandin E2 production were induced in those cells by increasing COX-2 promoter transcription activity, which could be attenuated by a specific p38MAPK inhibitor, suggesting a role for peritoneal fluid in the etiopathogenesis of endometriosis. Cell proliferation of endometrial stromal cells treated with peritoneal fluid of women (aged 25 to 43 years) with endometriosis (n = 12) statistically significantly increased compared with the control treatment (peritoneal fluid of women without endometriosis, n = 8). Also, COX-2 gene expression and prostaglandin E2 production were induced in those cells by increasing COX-2 promoter transcription activity, which could be attenuated by a specific p38MAPK inhibitor, suggesting a role for peritoneal fluid in the etiopathogenesis of endometriosis. Endometriosis is one of the most common benign disorders in women of reproductive age. Ectopic endometrial tissue generally exists within the pelvic peritoneum, in close contact with pelvic peritoneal fluid (PF). The role of the cellular population and soluble factors of PF has been extensively studied (1Loh F.H. Bongso A. Fong C.Y. Koh D.R. Lee S.H. Zhao H.Q. Effects of peritoneal macrophages from women with endometriosis on endometrial cellular proliferation in an in vitro coculture model.Fertil Steril. 1999; 72: 533-538Abstract Full Text Full Text PDF PubMed Scopus (23) Google Scholar), and recently, they have been reported to contribute to the implantation of endometrial cells and progress of endometrial lesions (2Castro J, Torres M, Sovino H, Fuentes A, Boric MA, Johnson MC. P450Arom induction in isolated control endometrial cells by peritoneal fluid from women with endometriosis. Fertil Steril. Published online April 27, 2010.Google Scholar). Of the active factors in PF, prostaglandins (PGs), particularly prostaglandin E2 (PGE2), can explain most of the symptoms of endometriosis (3Attar E. Bulun S.E. Aromatase and other steroidogenic genes in endometriosis: translational aspects.Hum Reprod Update. 2006; 12: 49-56Crossref PubMed Scopus (198) Google Scholar). Studies have suggested that COX-2 expression is increased in the eutopic endometria and ovarian endometriotic tissue of patients with endometriosis (4Cho S. Park S.H. Choi Y.S. Seo S.K. Kim H.Y. Park K.H. et al.Expression of cyclooxygenase-2 in eutopic endometrium and ovarian endometriotic tissue in women with severe endometriosis.Gynecol Obstet Invest. 2009; 69: 93-100Crossref PubMed Scopus (34) Google Scholar, 5Matsuzaki S. Canis M. Pouly J.L. Cyclooxygenase-2 expression in deep endometriosis and matched eutopic endometrium.Fertil Steril. 2004; 82: 1309-1315Abstract Full Text Full Text PDF PubMed Scopus (78) Google Scholar). Endometrial stromal cells (ESCs) are an important part of endometrial tissue, and their proliferation is closely related to the development of endometriosis. To date, however, the effects and mechanisms of PF in patients with endometriosis on the proliferation of ESCs is not well elucidated. The study participants were women undergoing diagnostic and/or therapeutic laparoscopy for endometriosis (6Meresman G.F. Barañao R.I. Tenenbaum A. Singla J.J. Neuspiller N.R. Rumi L.S. Effect of peritoneal fluid from patients with mild and severe endometriosis on endometrial stromal cell proliferation.Arch Gynecol Obstet. 1997; 259: 109-115Crossref PubMed Scopus (15) Google Scholar). After the laparoscopic examination, the patients (age range: 25 to 43 years) with endometriosis served as cases (n = 12), and those with no endometriosis served as the controls (n = 8). For isolation of ESCs, three tissue samples confirmed histologically as ovary cysts were obtained from three patients (ages 29, 42, and 31 years). All samples were obtained in the proliferative phase of the cycle. The consent forms and protocols used in our study were approved by the Human Investigation Committee of Changhai Hospital. The PF was centrifuged, and the supernatant was stored at –70°C. The isolated ESCs were cultured as described by Wang et al. (7Wang Y. Yu J. Luo X. Wang X. Li M. Wang L. Li D. Abnormal regulation of chemokine TECK and its receptor CCR9 in the endometriotic milieu is involved in pathogenesis of endometriosis by way of enhancing invasiveness of endometrial stromal cells.Cell Mol Immunol. 2010; 7: 51-60Crossref PubMed Scopus (30) Google Scholar). Cell proliferation of ESCs treated with PF at a final concentration of 10%, or 10 μM PGE2 or vehicle (dimethyl sulfoxide) was measured using the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) method. Secreted PGE2 levels of ESCs were quantified using a PGE2 monoclonal enzyme immunoassay kit (Cayman Chemical, Ann Arbor, MI). Total RNA was isolated and reverse transcribed. Real-time polymerase chain reaction (PCR) was performed using an ABI 7300 thermal cycler (Applied Biosystems, Foster City, CA). All primers were designed using the Primer Express program (Applied Biosystems). The relative expression of COX-2 gene compared with that of GAPDH was calculated using the 2–ΔΔCT method. The COX-2 protein level was confirmed by Western blot. Both COX-2 and GAPDH monoclonal antibodies were purchased from Cayman Chemical. Immunoreactive bands were visualized using an enhanced chemiluminescence detection system (Amersham PLC, Little Chalfont, Buckinghamshire, U.K.). For the reporter gene experiment, human COX-2 promoter (−1807 to +3) was amplified and cloned into the NheI–XhoI restriction sites of the luciferase reporter plasmid pGL3-Basic (Promega, Madison, WI). The ESCs were plated into 48-well plates for transient transfection experiments. The cells were transfected with pGL3-COX-2/renilla plasmids or control pGL3-Basic/renilla plasmids (1 μg/0.01 μg/well) using the FuGene 6 transfection reagent (Roche Applied Science, Branford, CT). After 4 hours of incubation, the transfection medium was changed, and 10% PF was added in the absence or presence of SB20358 (20 μM). The cells were then incubated for another 8 hours. The luciferase activity was measured with a GLOMAX Luminometer by using the Dual Luciferase Reporter Assay System (Promega). Data were represented as mean ± standard deviation (SD). Comparisons between the two groups were performed using the unpaired Student’s t test or the Mann-Whitney rank sum test. P<.05 was considered statistically significant. Institutional review board approval was obtained about this study. The purity of isolated ESCs was >95%, as determined by fluoroimmunoassay of vimentin (data not shown). To investigate whether the PF of patients with endometriosis contributed to the development of endometriosis, the effects of PF on the proliferation of three groups of isolated ESCs were analyzed. The addition of 10% PF obtained from patients with endometriosis or exogenous PGE2 (10 μM) to the cultures statistically significantly increased the proliferation of ESCs compared with CN PF or vehicle treatment groups (P<.05 and P<.01, respectively) (Fig. 1A). To determine the effects of PF on the expression levels of COX-2, we examined PGE2 production in the conditioned medium from cell cultures. The PF of patients with endometriosis caused a statistically significant increase in PGE2 secretion in ESCs compared with the control treatment (P<.05 and P<.01) (see Fig. 1B). Furthermore, the levels of COX-2 mRNA of ESCs were increased by the PF of patients with endometriosis when compared with the controls (P<.01) (see Fig. 1C), and a concomitant increase in COX-2 protein levels was observed by Western blot (see Fig. 1D). Additionally, a statistically significant increase in luciferase activity was observed after treatment with the PF of patients with endometriosis, which was attenuated by 20 μM SB203580, a specific p38MAPK inhibitor. These results were consistent in all three isolated samples of ESCs (see Fig. 1E). Previous studies have reported that the PF from patients with endometriosis promotes endometrial stromal cell proliferation in vitro. However, the mechanism for this effect was not further investigated and remains unknown (6Meresman G.F. Barañao R.I. Tenenbaum A. Singla J.J. Neuspiller N.R. Rumi L.S. Effect of peritoneal fluid from patients with mild and severe endometriosis on endometrial stromal cell proliferation.Arch Gynecol Obstet. 1997; 259: 109-115Crossref PubMed Scopus (15) Google Scholar, 8Surrey E.S. Halme J. Effect of peritoneal fluid from endometriosis patients on endometrial stromal cell proliferation in vitro.Obstet Gynecol. 1990; 76: 792-797Crossref PubMed Scopus (92) Google Scholar). We compared the effect of PF from patients with or without endometriosis on the proliferation of ESCs and calculated the dose-dependent and time-dependent curves (data not shown). The PF of patients with endometriosis had a much greater effect on the proliferation of ESCs than that of patients without endometriosis, but different isolated ESCs had subtle differences in their response to PF (P<.05 and P<.01). Our further investigation revealed that the PF of patients with endometriosis induced a statistically significant increase in COX-2 expression. These results suggest that PF of women with endometriosis may represent a favorable environment for ectopic endometrial implants. Our results are consistent with previous findings that macrophage migration inhibitory factor (MIF), which is elevated in the PF of patients with endometriosis, can induce COX-2 expression (9Carli C. Metz C.N. Al-Abed Y. Naccache P.H. Akoum A. Up-regulation of cyclooxygenase-2 expression and prostaglandin E2 production in human endometriotic cells by macrophage migration inhibitory factor: involvement of novel kinase signaling pathways.Endocrinology. 2009; 150: 3128-3137Crossref PubMed Scopus (81) Google Scholar). The mitogen-activated protein kinase (MAPK) pathway is an important intracellular signal transduction system that is involved in gene transcription, cell growth, cell development and differentiation, apoptosis, and a series of pathological processes (10Cano E. Mahadevan L.C. Parallel signal processing among mammalian MAPKs.Trends Biochem Sci. 1995; 20: 117-122Abstract Full Text PDF PubMed Scopus (996) Google Scholar, 11Gallo K.A. Johnson G.L. Mixed-lineage kinase control of JNK and p38 MAPK pathways.Nat Rev Mol Cell Biol. 2002; 3: 663-672Crossref PubMed Scopus (448) Google Scholar). However, a specific p38MAPK inhibitor, SB203580, may interrupt kinase activation by the MAPK pathway. Our data show that the PF of patients with endometriosis enhances COX-2 promoter transcription activity in a statistically significant manner, but the effects can be blocked partially by SB203580. This result indicates that additional pathways may participate in PF-induced COX-2 gene expression. Our results have shown that the PF of patients with endometriosis promotes the proliferation of ESCs, suggesting a role for PF in the etiopathogenesis of endometriosis. Furthermore, this PF can also induce COX-2 gene expression and enhance PGE2 secretion in ESCs, and a part of this effect is mediated via the MAPK pathway." @default.
• W2055069536 created "2016-06-24" @default.
• W2055069536 creator A5006716573 @default.
• W2055069536 creator A5025938022 @default.
• W2055069536 creator A5029762841 @default.
• W2055069536 creator A5031911074 @default.
• W2055069536 creator A5056248574 @default.
• W2055069536 creator A5058357427 @default.
• W2055069536 creator A5061544635 @default.
• W2055069536 creator A5068442102 @default.
• W2055069536 creator A5089639451 @default.
• W2055069536 date "2011-04-01" @default.
• W2055069536 modified "2023-10-13" @default.
• W2055069536 title "Peritoneal fluid of patients with endometriosis promotes proliferation of endometrial stromal cells and induces COX-2 expression" @default.
• W2055069536 cites W2014647766 @default.
• W2055069536 cites W2022333403 @default.
• W2055069536 cites W2033126075 @default.
• W2055069536 cites W2047559975 @default.
• W2055069536 cites W2054671913 @default.
• W2055069536 cites W2060063893 @default.
• W2055069536 cites W2073541193 @default.
• W2055069536 cites W2078909544 @default.
• W2055069536 cites W2084666971 @default.
• W2055069536 cites W2143048167 @default.
• W2055069536 cites W2790805946 @default.
• W2055069536 doi "https://doi.org/10.1016/j.fertnstert.2010.11.039" @default.
• W2055069536 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21145050" @default.
• W2055069536 hasPublicationYear "2011" @default.
• W2055069536 type Work @default.
• W2055069536 sameAs 2055069536 @default.
• W2055069536 citedByCount "15" @default.
• W2055069536 countsByYear W20550695362012 @default.
• W2055069536 countsByYear W20550695362013 @default.
• W2055069536 countsByYear W20550695362014 @default.
• W2055069536 countsByYear W20550695362015 @default.
• W2055069536 countsByYear W20550695362017 @default.
• W2055069536 countsByYear W20550695362018 @default.
• W2055069536 countsByYear W20550695362019 @default.
• W2055069536 countsByYear W20550695362021 @default.
• W2055069536 countsByYear W20550695362022 @default.
• W2055069536 crossrefType "journal-article" @default.
• W2055069536 hasAuthorship W2055069536A5006716573 @default.
• W2055069536 hasAuthorship W2055069536A5025938022 @default.
• W2055069536 hasAuthorship W2055069536A5029762841 @default.
• W2055069536 hasAuthorship W2055069536A5031911074 @default.
• W2055069536 hasAuthorship W2055069536A5056248574 @default.
• W2055069536 hasAuthorship W2055069536A5058357427 @default.
• W2055069536 hasAuthorship W2055069536A5061544635 @default.
• W2055069536 hasAuthorship W2055069536A5068442102 @default.
• W2055069536 hasAuthorship W2055069536A5089639451 @default.
• W2055069536 hasBestOaLocation W20550695361 @default.
• W2055069536 hasConcept C126322002 @default.
• W2055069536 hasConcept C143998085 @default.
• W2055069536 hasConcept C16685009 @default.
• W2055069536 hasConcept C16930146 @default.
• W2055069536 hasConcept C2779522080 @default.
• W2055069536 hasConcept C29456083 @default.
• W2055069536 hasConcept C502942594 @default.
• W2055069536 hasConcept C71924100 @default.
• W2055069536 hasConcept C98055416 @default.
• W2055069536 hasConceptScore W2055069536C126322002 @default.
• W2055069536 hasConceptScore W2055069536C143998085 @default.
• W2055069536 hasConceptScore W2055069536C16685009 @default.
• W2055069536 hasConceptScore W2055069536C16930146 @default.
• W2055069536 hasConceptScore W2055069536C2779522080 @default.
• W2055069536 hasConceptScore W2055069536C29456083 @default.
• W2055069536 hasConceptScore W2055069536C502942594 @default.
• W2055069536 hasConceptScore W2055069536C71924100 @default.
• W2055069536 hasConceptScore W2055069536C98055416 @default.
• W2055069536 hasIssue "5" @default.
• W2055069536 hasLocation W20550695361 @default.
• W2055069536 hasLocation W20550695362 @default.
• W2055069536 hasOpenAccess W2055069536 @default.
• W2055069536 hasPrimaryLocation W20550695361 @default.
• W2055069536 hasRelatedWork W1978598833 @default.
• W2055069536 hasRelatedWork W2039922632 @default.
• W2055069536 hasRelatedWork W2047559975 @default.
• W2055069536 hasRelatedWork W2053341807 @default.
• W2055069536 hasRelatedWork W2054671913 @default.
• W2055069536 hasRelatedWork W2055069536 @default.
• W2055069536 hasRelatedWork W2084146249 @default.
• W2055069536 hasRelatedWork W2127420749 @default.
• W2055069536 hasRelatedWork W2355997651 @default.
• W2055069536 hasRelatedWork W2898589616 @default.
• W2055069536 hasVolume "95" @default.
• W2055069536 isParatext "false" @default.
• W2055069536 isRetracted "false" @default.
• W2055069536 magId "2055069536" @default.
• W2055069536 workType "article" @default.