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• W2005650140 abstract "Significantly higher levels of prostaglandin E2 and vascular endothelial growth factor were associated with the severity of endometriosis. In this study, pathologic concentrations of prostaglandin E2 and vascular endothelial growth factor found in endometriotic women significantly inhibited sperm motility, acrosome reaction, and sperm–oocyte interaction, which might result in endometriosis-associated subfertility/infertility. Significantly higher levels of prostaglandin E2 and vascular endothelial growth factor were associated with the severity of endometriosis. In this study, pathologic concentrations of prostaglandin E2 and vascular endothelial growth factor found in endometriotic women significantly inhibited sperm motility, acrosome reaction, and sperm–oocyte interaction, which might result in endometriosis-associated subfertility/infertility. Endometriosis, the presence of endometrial tissue outside the uterus, is usually associated with reduced fertility. Besides anatomic factors caused by endometriosis, such as ovarian cysts and obstruction of oviducts, it is now widely accepted that immunologic factors are involved in the pathophysiology of endometriosis-associated infertility (1Berkkanoglu M. Arici A. Immunology and endometriosis.Am J Reprod Immunol. 2003; 50: 48-59Crossref PubMed Scopus (180) Google Scholar). Endometriosis-associated immunoinflammatory changes may have adverse effects on sperm because they have to stay for a period of time in the female reproductive tract. The female reproductive environment is bathed by peritoneal fluid, the immunologic composition of which changes greatly during endometriosis (1Berkkanoglu M. Arici A. Immunology and endometriosis.Am J Reprod Immunol. 2003; 50: 48-59Crossref PubMed Scopus (180) Google Scholar). Activated macrophages increase in the peritoneal fluid of endometriotic women. Macrophages may contribute to endometriosis-associated infertility directly by sperm phagocytosis or indirectly by secreting cytokines/factors that affect sperm or the patient’s reproductive function (2Harada T. Iwabe T. Terakawa N. Role of cytokines in endometriosis.Fertil Steril. 2001; 76: 1-10Abstract Full Text Full Text PDF PubMed Scopus (369) Google Scholar). For example, overproduction of interleukin-1 and prostaglandins was shown to have deleterious effects on embryonic implantation and development (3Oral E. Olive D.L. Arici A. The peritoneal environment in endometriosis.Hum Reprod Update. 1996; 2: 385-398Crossref PubMed Scopus (168) Google Scholar). Angiogenesis plays a key role in the establishment and growth of endometriotic lesions. Vascular endothelial growth factor (VEGF) is a potent proangiogenic factor, and significantly higher levels of VEGF were found in active sites of endometriotic lesions. Elevated prostaglandin E2 (PGE2) was found to increase VEGF expression in the peritoneal fluid and lesions of endometriotic patients compared with controls (4Becker C.M. D’Amato R.J. Angiogenesis and antiangiogenic therapy in endometriosis.Microvasc Res. 2007; 74: 121-130Crossref PubMed Scopus (98) Google Scholar). Interestingly, cyclooxygenase-2, an enzyme that functions to generate prostaglandins involved in inflammatory processes, is also up-regulated in the endometrium of endometriotic patients (5Ota H. Igarashi S. Sasaki M. Tanaka T. Distribution of cyclooxygenase-2 in eutopic and ectopic endometrium in endometriosis and adenomyosis.Hum Reprod. 2001; 16: 561-566Crossref PubMed Scopus (269) Google Scholar). Therefore, increased cyclooxygenase-2 in endometriotic patients could lead to higher PGE2 levels and have a direct effect on angiogenesis by enhancing VEGF expression. Prostaglandin E2 increases dramatically in the peritoneal fluid of endometriotic women, and the concentration of PGE2 has been correlated with severity of endometriotic lesions (6Li Z.G. Lang J.H. Leng J.H. Liu D.Y. Increased levels of prostaglandin E2 and bcl-2 in peritoneal fluid and serum of patients with endometriosis.Zhonghua Fu Chan Ke Za Zhi. 2005; 40: 598-600PubMed Google Scholar). The association of increased PGE2 and VEGF with endometriosis is prominent. However, the specific effect of PGE2 or VEGF on sperm has not been described, especially for events occurring in the female reproductive tract, such as the acrosome reaction (AR) and sperm–egg interaction. To understand endometriosis-associated infertility, the role of PGE2 and VEGF, both important in endometriotic angiogenesis, should be clarified. Written informed consent was obtained from seven normozoospermic donors according to World Health Organization (WHO) guidelines (7World Health OrganizationWHO laboratory manual for the examination of human semen and sperm-cervical mucus interaction.4th ed. Cambridge University Press, Cambridge, United Kingdom1999Google Scholar). The research protocol was approved by the institutional review board of the Yu-Li Veterans Hospital. Semen was obtained by masturbation from donors after a minimum of 3 days of sexual abstinence. Motile sperm were collected by swim-up in Biggers-Whitten-Whittingham medium (7World Health OrganizationWHO laboratory manual for the examination of human semen and sperm-cervical mucus interaction.4th ed. Cambridge University Press, Cambridge, United Kingdom1999Google Scholar). Sperm were treated with various concentrations of PGE2, VEGF, or vehicle as control. Motility was assessed at 37°C by computer-assisted sperm analysis system (Integrated Semen Analysis System, Proiser, Spain). Sperm were categorized according to WHO criteria. Percentage of progressive sperm included sperm with velocity >5 μm/s. Sperm treated with PGE2, VEGF, or vehicle were capacitated for 20 hours at 37°C, 5% CO2. Samples were treated either with 10 μM A23187 to induce AR or with 0.1% dimethyl sulfoxide (vehicle) to detect spontaneous AR. Acrosomal status was evaluated by Pisum sativum agglutinin conjugated to fluorescein isothiocyanate (8Cross N.L. Meizel S. Methods for evaluating the acrosomal status of mammalian sperm.Biol Reprod. 1989; 41: 635-641Crossref PubMed Scopus (169) Google Scholar). A zona-free hamster egg penetration test was carried out according to WHO guidelines (7World Health OrganizationWHO laboratory manual for the examination of human semen and sperm-cervical mucus interaction.4th ed. Cambridge University Press, Cambridge, United Kingdom1999Google Scholar). Sperm treated with PGE2 or VEGF, capacitated for 20 hours, were incubated with A23187 to induce AR. Sperm were coincubated with oocytes at 37°C for 3 hours. Sperm penetration index (SPI) was calculated as the mean number of sperm penetrating each oocyte. Data are expressed as mean ± SD. Statistical analysis was performed with SPSS statistical software (SPSS, Chicago, IL). One-way analysis of variance, followed by post hoc comparisons with least significant difference test, was used to compare differences among treatment groups. A P value of <.05 was considered statistically significant. Table 1 summarizes the effects of PGE2 and VEGF on sperm function. Sperm motility was evaluated every 45 minutes for 3 hours. Prostaglandin E2 did not affect sperm motility. However, VEGF affected sperm motility and progressivity in a time- and dose-dependent manner. Percentages of motile and progressive sperm decreased significantly when sperm were incubated with high concentrations (10 and 100 ng/mL) of VEGF for >2 hours (vs. control, P<.01).Table 1Effects of PGE2 and VEGF on sperm function.PGE2 concentration (ng/mL)VEGF concentration (ng/mL)Variable00.222020000.1110100Motility (%) 0 min92 ± 3.7493 ± 2.6693 ± 4.4693 ± 2.1491 ± 4.9296 ± 3.6695 ± 4.9695 ± 2.9295 ± 2.5394 ± 2.38 45 min93 ± 3.8294 ± 3.2792 ± 3.2790 ± 5.2493 ± 3.3395 ± 3.2595 ± 3.1895 ± 3.3093 ± 3.9694 ± 2.78 90 min93 ± 3.7693 ± 2.3591 ± 2.8392 ± 4.6791 ± 4.9795 ± 2.2596 ± 3.8995 ± 2.7093 ± 4.6690 ± 4.93 135 min93 ± 3.2091 ± 4.5891 ± 4.1393 ± 2.3292 ± 3.1495 ± 3.4894 ± 4.1494 ± 2.1288 ± 1.69aSignificantly different from control group, P<.01.84 ± 1.13aSignificantly different from control group, P<.01. 180 min93 ± 4.1892 ± 2.3792 ± 3.1991 ± 2.8192 ± 2.5694 ± 1.6094 ± 2.0391 ± 2.2687 ± 3.00aSignificantly different from control group, P<.01.82 ± 5.90aSignificantly different from control group, P<.01.Progressivity (%) 0 min87 ± 5.5689 ± 3.6988 ± 4.7389 ± 2.3287 ± 6.0990 ± 5.6891 ± 5.9591 ± 3.5492 ± 3.3889 ± 3.58 45 min89 ± 5.1388 ± 4.3686 ± 4.7285 ± 5.6189 ± 4.0291 ± 4.7491 ± 5.1390 ± 4.6989 ± 4.4790 ± 4.13 90 min89 ± 3.9488 ± 3.7287 ± 3.4987 ± 5.1986 ± 6.1991 ± 2.7791 ± 4.4689 ± 4.7787 ± 7.4084 ± 7.27 135 min89 ± 4.2488 ± 5.2486 ± 6.3188 ± 2.9388 ± 4.0290 ± 5.3791 ± 4.9390 ± 3.6281 ± 3.54aSignificantly different from control group, P<.01.76 ± 2.36aSignificantly different from control group, P<.01. 180 min88 ± 5.7388 ± 3.4988 ± 3.6086 ± 2.7388 ± 3.3590 ± 2.4589 ± 2.0087 ± 3.4683 ± 4.38aSignificantly different from control group, P<.01.74 ± 7.42aSignificantly different from control group, P<.01.AR (%) Spontaneous20.7 ± 5.4817.9 ± 5.3513.5 ± 3.92bSignificantly different from control group, P<.05.9.9 ± 3.61bSignificantly different from control group, P<.05.9.0 ± 4.80bSignificantly different from control group, P<.05.23.4 ± 2.0119.4 ± 2.5419.0 ± 2.9813.7 ± 2.35bSignificantly different from control group, P<.05.12.3 ± 2.18bSignificantly different from control group, P<.05. A23187-induced41.7 ± 7.8439.3 ± 9.4827.4 ± 7.76bSignificantly different from control group, P<.05.17.6 ± 8.48bSignificantly different from control group, P<.05.12.5 ± 6.72bSignificantly different from control group, P<.05.46.3 ± 3.6744.1 ± 1.7539.7 ± 3.3828.0 ± 5.24bSignificantly different from control group, P<.05.23.4 ± 4.45bSignificantly different from control group, P<.05.Egg penetration SPI3.62 ± 0.903.67 ± 0.842.27 ± 0.82bSignificantly different from control group, P<.05.1.92 ± 0.73bSignificantly different from control group, P<.05.1.51 ± 0.32bSignificantly different from control group, P<.05.3.74 ± 0.513.50 ± 0.493.28 ± 0.552.53 ± 0.22bSignificantly different from control group, P<.05.1.40 ± 0.23bSignificantly different from control group, P<.05. RangecRange of mean SPI from four (PGE2) or five (VEGF) replicates.2.30–4.252.45–4.401.60–3.461.33–2.921.18–1.913.29–4.272.93–4.002.56–3.882.25–2.791.08–1.58Note: Values are mean ± SD unless otherwise noted.a Significantly different from control group, P<.01.b Significantly different from control group, P<.05.c Range of mean SPI from four (PGE2) or five (VEGF) replicates. Open table in a new tab Note: Values are mean ± SD unless otherwise noted. Sperm capacitation was evaluated by the ability to undergo AR. A statistically significant reduction of AR was observed at high concentrations of PGE2 (2, 20, and 200 ng/mL, P< .05) and VEGF (10 and 100 ng/mL, P<.05). However, low concentrations of PGE2 and VEGF treatment showed similar effects on AR as control (vehicle treated). Consistent with the results described above, low concentrations of PGE2 (0.2 ng/mL) and VEGF (0.1 and 1 ng/mL) did not interfere with sperm–oocyte interaction; the SPI ranged from 3.28 ± 0.55 to 3.74 ± 0.51 (P>.05). However, both PGE2 and VEGF at high concentrations significantly reduced SPI; the higher the concentrations, the lower the SPI (1.51 ± 0.32 at PGE2 200 ng/mL; 1.40 ± 0.23 at VEGF 100 ng/mL). Sperm have to reside in the female reproductive tract for a specific period of time to acquire the ability to fertilize eggs. This phenomenon, called capacitation, is supported by endometrial and ovarian epithelial cells. Therefore, besides normal sperm function, a healthy female reproductive tract is essential for successful fertilization. In endometriotic women, the PGE2 level in peritoneal fluid and infertility are correlated with the severity of disease (6Li Z.G. Lang J.H. Leng J.H. Liu D.Y. Increased levels of prostaglandin E2 and bcl-2 in peritoneal fluid and serum of patients with endometriosis.Zhonghua Fu Chan Ke Za Zhi. 2005; 40: 598-600PubMed Google Scholar). As intraperitoneal PGE2 reaches 2 ng/mL, which is equivalent to the level in ascites of patients with moderate endometriosis, a clinically obvious decline of fertility can be expected. Interestingly, we found decreased percentages of AR and oocyte penetration when sperm were exposed to pathologic levels (≥2 ng/mL) of PGE2. Conversely, sperm treated with PGE2 at the physiologic range, such as 0.2 ng/mL, behaved as normal as control. Hence fertility was not changed; this is compatible with clinical observations. The concentration of VEGF in the peritoneal fluid of endometriotic patients varies greatly and is related to the menstrual cycle and stage of disease (4Becker C.M. D’Amato R.J. Angiogenesis and antiangiogenic therapy in endometriosis.Microvasc Res. 2007; 74: 121-130Crossref PubMed Scopus (98) Google Scholar). However, it is reasonable to consider that 10–100 ng/mL of VEGF exceeds the pathologic level, whereas <1 ng/mL of VEGF should be in the physiologic range (9Shifren J.L. Tseng J.F. Zaloudek C.J. Ryan I.P. Meng Y.G. Ferrara N. et al.Ovarian steroid regulation of vascular endothelial growth factor in the human endometrium: implications for angiogenesis during the menstrual cycle and in the pathogenesis of endometriosis.J Clin Endocrinol Metab. 1996; 81: 3112-3118Crossref PubMed Scopus (625) Google Scholar). This is in accordance with our findings that sperm function was affected by VEGF at 10–100 ng/mL, whereas sperm exposed to a physiologic range of VEGF were not affected. Other cytokines related to endometriosis also show similar dual effects on sperm. For example, macrophage migration inhibitory factor inhibits sperm capacitation at high concentrations but favors capacitation at low concentrations (10Carli C. Leclerc P. Metz C.N. Akoum A. Direct effect of macrophage migration inhibitory factor on sperm function: possible involvement in endometriosis-associated infertility.Fertil Steril. 2007; 88: 1240-1247Abstract Full Text Full Text PDF PubMed Scopus (31) Google Scholar). From this study, we propose that PGE2 or VEGF could serve as a therapeutic index. Cancer antigen 125 (CA-125) is often used as an endometriotic marker, and its concentration may reflect disease severity, but CA-125 may elevate in other pathologic conditions, such as pelvic inflammatory adhesions and ovarian cancer (11Ghaemmaghami F. Karimi Zarchi M. Hamedi B. High levels of CA125 (over 1,000 IU/ml) in patients with gynecologic disease and no malignant conditions: three cases and literature review.Arch Gynecol Obstet. 2007; 276: 559-561Crossref PubMed Scopus (26) Google Scholar). Therefore, the results of CA-125 measurement must be interpreted carefully. Recently, high-sensitivity C-reactive protein was proposed to serve as a marker for the absence of endometriosis; however, no differences were found between different disease stages (12Lermann J. Mueller A. Körber F. Oppelt P. Beckmann M.W. Dittrich R. et al.Evaluation of high-sensitivity C-reactive protein in comparison with C-reactive protein as biochemical serum markers in women with endometriosis.Fertil Steril. 2010; 93: 2125-2129Abstract Full Text Full Text PDF PubMed Scopus (28) Google Scholar). Because PGE2 and VEGF were significantly higher in patients with endometriosis and had positive correlations with severity of disease, in theory they could feasibly be used as a therapeutic index. Effects on infertility could also be estimated. In conclusion, this study showed that pathologic concentrations of PGE2 and VEGF both inhibited sperm function. Therefore, bathing of sperm in an environment with high PGE2 or VEGF, as is the case in endometriotic patients, may result in suppressed sperm function and lead to subfertility/infertility." @default.
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• W2005650140 title "Effects of prostaglandin E2 and vascular endothelial growth factor on sperm might lead to endometriosis-associated infertility" @default.
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