全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...

Interplay between Misplaced Müllerian-Derived Stem Cells and Peritoneal Immune Dysregulation in the Pathogenesis of Endometriosis

DOI: 10.1155/2013/527041

Full-Text   Cite this paper   Add to My Lib

Abstract:

In the genetic regulation of Müllerian structures development, a key role is played by Hoxa and Wnt clusters, because they lead the transcription of different genes according to the different phases of the organogenesis, addressing correctly cell-to-cell interactions, allowing, finally, the physiologic morphogenesis. Accumulating evidence is suggesting that dysregulation of Wnt and/or Hox genes may affect cell migration during organogenesis and differentiation of Müllerian structures of the female reproductive tract, with possible dislocation and dissemination of primordial endometrial stem cells in ectopic regions, which have high plasticity to differentiation. We hypothesize that during postpubertal age, under the influence of different stimuli, these misplaced and quiescent ectopic endometrial cells could acquire new phenotype, biological functions, and immunogenicity. So, these kinds of cells may differentiate, specializing in epithelium, glands, and stroma to form a functional ectopic endometrial tissue. This may provoke a breakdown in the peritoneal cavity homeostasis, with the consequent processes of immune alteration, documented by peripheral mononuclear cells recruitment and secretion of inflammatory cytokines in early phases and of angiogenic and fibrogenic cytokines in the late stages of the disease. 1. Introduction Endometriosis is an estrogen-dependent disease [1] characterized by the ectopic presence and growth of functional endometrial tissue, glands, and stroma, outside the uterine cavity [2, 3]. It affects deeply and negatively woman’s quality of life, contributing not only to suffering but also to marital and family problems, to problems related to the achievements of work tasks, and overall to disability in woman’s role in modern society [4–7]. Its treatment, medical or surgical depending on each case, on the contrary, could improve and partially restore women’s health-related quality of life (HRQoL), like is reported by Jia et al. [8] and Gao et al. [9]. Risk factors for this disease are nulliparity, high education level, and social class (probably because these patients undergo accurate medical controls more easily) [10], although it is widespread across countries and ethnicities, and women continue to experience diagnostic delays in primary care [6]. As is suggested by many authors [11, 12] the risk of endometriosis appears to increase for reproductive health factors that may relate to increased exposure to menstruation (i.e., shorter cycle length, longer duration of flow, or reduced parity). The risk appears to decrease for

References

[1]  L. C. Giudice and L. C. Kao, “Endometriosis,” The Lancet, vol. 364, no. 9447, pp. 1789–1799, 2004.
[2]  A. Baldi, M. Campioni, and P. G. Signorile, “Endometriosis: pathogenesis, diagnosis, therapy and association with cancer,” Oncology Reports, vol. 19, no. 4, pp. 843–846, 2008.
[3]  S. E. Bulun, “Endometriosis,” The New England Journal of Medicine, vol. 360, no. 3, pp. 268–279, 2009.
[4]  J. Fourquet, L. Báez, M. Figueroa, R. I. Iriarte, and I. Flores, “Quantification of the impact of endometriosis symptoms on health-related quality of life and work productivity,” Fertility and Sterility, vol. 96, no. 1, pp. 107–112, 2011.
[5]  G. Jones, C. Jenkinson, and S. Kennedy, “The impact of endometriosis upon quality of life: a qualitative analysis,” Journal of Psychosomatic Obstetrics and Gynecology, vol. 25, no. 2, pp. 123–133, 2004.
[6]  K. E. Nnoaham, L. Hummelshoj, P. Webster et al., “Impact of endometriosis on quality of life and work productivity: a multicenter study across ten countries,” Fertility and Sterility, vol. 96, no. 2, pp. 366.e8–373.e8, 2011.
[7]  M. Fanta, P. Koliba, and H. Hru?ková, “Endometriosis,” Ceska Gynekol, vol. 77, no. 4, pp. 314–319, 2012.
[8]  S. Z. Jia, J. H. Leng, J. H. Shi, P. R. Sun, and J. H. Lang, “Health-related quality of life in women with endometriosis: a systematic review,” Journal of Ovarian Research, vol. 5, no. 1, p. 29, 2012.
[9]  X. Gao, Y.-C. Yeh, J. Outley, J. Simon, M. Botteman, and J. Spalding, “Health-related quality of life burden of women with endometriosis: a literature review,” Current Medical Research and Opinion, vol. 22, no. 9, pp. 1787–1797, 2006.
[10]  R. Hemmings, M. Rivard, D. L. Olive et al., “Evaluation of risk factors associated with endometriosis,” Fertility and Sterility, vol. 81, no. 6, pp. 1513–1521, 2004.
[11]  B. Eskenazi and M. L. Warner, “Epidemiology of endometriosis,” Obstetrics and Gynecology Clinics of North America, vol. 24, no. 2, pp. 235–258, 1997.
[12]  P. Viganò, F. Parazzini, E. Somigliana, and P. Vercellini, “Endometriosis: epidemiology and aetiological factors,” Best Practice and Research, vol. 18, no. 2, pp. 177–200, 2004.
[13]  K. Huhtinen, A. Perheentupa, M. Poutanen, and O. Heikinheimo, “Pathogenesis of endometriosis,” Duodecim, vol. 127, no. 17, pp. 1827–1835, 2011.
[14]  R. Marana, A. Lecca, A. Biscione, and E. L. Muzii, “Endometriosis: the gynecologist's opinion,” Urologia, vol. 79, no. 3, pp. 160–166, 2012.
[15]  P. Stratton and K. J. Berkley, “Chronic pelvic pain and endometriosis: translational evidence of the relationship and implications,” Human Reproduction Update, vol. 17, no. 3, pp. 327–346, 2011.
[16]  A. Fauconnier, X. Fritel, and C. Chapron, “Endometriosis and pelvic pain: epidemiological evidence of the relationship and implications,” Gynecologie Obstetrique Fertilite, vol. 37, no. 1, pp. 57–69, 2009.
[17]  M. G. Porpora, P. R. Koninckx, J. Piazze, M. Natili, S. Colagrande, and E. V. Cosmi, “Correlation between endometriosis and pelvic pain,” Journal of the American Association of Gynecologic Laparoscopists, vol. 6, no. 4, pp. 429–434, 1999.
[18]  P. Vercellini, L. Fedele, G. Aimi, G. Pietropaolo, D. Consonni, and P. G. Crosignani, “Association between endometriosis stage, lesion type, patient characteristics and severity of pelvic pain symptoms: a multivariate analysis of over 1000 patients,” Human Reproduction, vol. 22, no. 1, pp. 266–271, 2007.
[19]  M. S. Arruda, C. A. Petta, M. S. Abr?o, and C. L. Benetti-Pinto, “Time elapsed from onset of symptoms to diagnosis of endometriosis in a cohort study of Brazilian women,” Human Reproduction, vol. 18, no. 4, pp. 756–759, 2003.
[20]  K. J. Berkley, A. J. Rapkin, and R. E. Papka, “The pains of endometriosis,” Science, vol. 308, no. 5728, pp. 1587–1589, 2005.
[21]  O. L. Westney, C. L. Amundsen, and E. J. Mcguire, “Bladder endometriosis: conservative management,” Journal of Urology, vol. 163, no. 6, pp. 1814–1817, 2000.
[22]  E. T. Tra?c?, E. Tra?c?, A. Ti?u, M. L. Riza, and I. Busuioc, “Ureteral stenosis due to endometriosis,” Romanian Journal of Morphology and Embryology, vol. 53, no. 2, pp. 433–437, 2012.
[23]  T. E. Shook and L. M. Nyberg, “Endometriosis of the urinary tract,” Urology, vol. 31, no. 1, pp. 1–6, 1988.
[24]  C. Sinder, G. R. Dochat, and N. E. Wentsler, “Splenoendometriosis,” American Journal of Obstetrics and Gynecology, vol. 92, pp. 883–884, 1965.
[25]  K. Saadat-Gilani, L. Bechmann, A. Frilling, G. Gerken, and A. Canbay, “Gallbladder endometriosis as a cause of occult bleeding,” World Journal of Gastroenterology, vol. 13, no. 33, pp. 4517–4519, 2007.
[26]  K. Kyamidis, V. Lora, and J. Kanitakis, “Spontaneous cutaneous umbilical endometriosis: report of a new case with immunohistochemical study and literature review,” Dermatology Online Journal, vol. 17, no. 7, p. 5, 2011.
[27]  American Society for Reproductive Medicine, “Revised American society for reproductive medicine classification of endometriosis,” Fertility and Sterility, vol. 67, no. 5, pp. 817–821, 1997.
[28]  A. Capobianco and P. Rovere-Querini, “Endometriosis, a disease of the macrophage,” Frontiers in Immunology, vol. 4, article 9, 2013.
[29]  K. A. Smith, C. B. Pearson, A. M. Hachey, D. L. Xia, and L. M. Wachtman, “Alternative activation of macrophages in rhesus macaques (Macaca mulatta) with endometriosis,” Comparative Medicine, vol. 62, no. 4, pp. 303–310, 2012.
[30]  K. J. Mylonas, M. G. Nair, L. Prieto-Lafuente, D. Paape, and J. E. Allen, “Alternatively activated macrophages elicited by helminth infection can be reprogrammed to enable microbial killing,” Journal of Immunology, vol. 182, no. 5, pp. 3084–3094, 2009.
[31]  A. Arici, E. Oral, E. Attar, S. I. Tazuke, and D. L. Olive, “Monocyte chemotactic protein-1 concentration in peritoneal fluid of women with endometriosis and its modulation of expression in mesothelial cells,” Fertility and Sterility, vol. 67, no. 6, pp. 1065–1072, 1997.
[32]  D. P. Braun, J. Ding, J. Shen, N. Rana, B. B. Fernandez, and W. P. Dmowski, “Relationship between apoptosis and the number of macrophages in eutopic endometrium from women with and without endometriosis,” Fertility and Sterility, vol. 78, no. 4, pp. 830–835, 2002.
[33]  X. Cao, D. Yang, M. Song, A. Murphy, and S. Parthasarathy, “The presence of endometrial cells in the peritoneal cavity enhances monocyte recruitment and induces inflammatory cytokines in mice: implications for endometriosis,” Fertility and Sterility, vol. 82, supplement 3, pp. 999–1007, 2004.
[34]  A. Pizzo, F. M. Salmeri, F. V. Ardita, V. Sofo, M. Tripepi, and S. Marsico, “Behaviour of cytokine levels in serum and peritoneal fluid of women with endometriosis,” Gynecologic and Obstetric Investigation, vol. 54, no. 2, pp. 82–87, 2002.
[35]  N. Tariverdian, F. Siedentopf, M. Rücke et al., “Intraperitoneal immune cell status in infertile women with and without endometriosis,” Journal of Reproductive Immunology, vol. 80, no. 1-2, pp. 80–90, 2009.
[36]  L. Galleri, S. Luisi, M. Rotondi et al., “Low serum and peritoneal fluid concentration of interferon-γ-induced protein-10 (CXCL10) in women with endometriosis,” Fertility and Sterility, vol. 91, no. 2, pp. 331–334, 2009.
[37]  J.-C. Lousse, S. Defrère, A. Van Langendonckt et al., “Iron storage is significantly increased in peritoneal macrophages of endometriosis patients and correlates with iron overload in peritoneal fluid,” Fertility and Sterility, vol. 91, no. 5, pp. 1668–1675, 2009.
[38]  R. Novembri, P. Carrarelli, P. Toti et al., “Urocortin 2 and urocortin 3 inendometriosis: evidence for a possible role in inflammatory response,” Molecular Human Reproduction, vol. 17, no. 9, pp. 587–593, 2011.
[39]  P.-C. Chuang, M.-H. Wu, Y. Shoji, and S.-J. Tsai, “Downregulation of CD36 results in reduced phagocytic ability of peritoneal macrophages of women with endometriosis,” The Journal of Pathology, vol. 219, no. 2, pp. 232–241, 2009.
[40]  P.-C. Chuang, Y.-J. Lin, M.-H. Wu, L.-Y. C. Wing, Y. Shoji, and S.-J. Tsai, “Inhibition of CD36-dependent phagocytosis by prostaglandin E2 contributes to the development of endometriosis,” The American Journal of Pathology, vol. 176, no. 2, pp. 850–860, 2010.
[41]  M. Bacci, A. Capobianco, A. Monno et al., “Macrophages are alternatively activated in patients with endometriosis and required for growth and vascularization of lesions in a mouse model of disease,” The American Journal of Pathology, vol. 175, no. 2, pp. 547–556, 2009.
[42]  J. T. Borda, X. Alvarez, M. Mohan et al., “CD163, a marker of perivascular macrophages, is up-regulated by microglia in simian immunodeficiency virus encephalitis after haptoglobin-hemoglobin complex stimulation and is suggestive of breakdown of the blood-brain barrier,” The American Journal of Pathology, vol. 172, no. 3, pp. 725–737, 2008.
[43]  G. Cairo, S. Recalcati, A. Mantovani, and M. Locati, “Iron trafficking and metabolism in macrophages: contribution to the polarized phenotype,” Trends in Immunology, vol. 32, no. 6, pp. 241–247, 2011.
[44]  S. Recalcati, M. Locati, A. Marini et al., “Differential regulation of iron homeostasis during human macrophage polarized activation,” European Journal of Immunology, vol. 40, no. 3, pp. 824–835, 2010.
[45]  J.-P. Bach, B. Rinn, B. Meyer, R. Dodel, and M. Bacher, “Role of MIF in inflammation and tumorigenesis,” Oncology, vol. 75, no. 3-4, pp. 127–133, 2008.
[46]  K. Khoufache, S. Bazin, K. Girard, et al., “Macrophage migration inhibitory factor antagonist blocks the development of endometriosis in vivo,” PLoS One, vol. 7, no. 5, Article ID e37264, 2012.
[47]  A. Akoum, C. N. Metz, M. Al-Akoum, and R. Kats, “Macrophage migration inhibitory factor expression in the intrauterine endometrium of women with endometriosis varies with disease stage, infertility status, and pelvic pain,” Fertility and Sterility, vol. 85, no. 5, pp. 1379–1385, 2006.
[48]  B. Seeber, M. D. Sammel, X. Fan et al., “Panel of markers can accurately predict endometriosis in a subset of patients,” Fertility and Sterility, vol. 89, no. 5, pp. 1073–1081, 2008.
[49]  C. Carli, C. N. Metz, Y. Al-Abed, P. H. Naccache, and A. Akoum, “Up-regulation of cyclooxygenase-2 expression and prostaglandin E 2 production in human endometriotic cells by macrophage migration inhibitory factor: involvement of novel kinase signaling pathways,” Endocrinology, vol. 150, no. 7, pp. 3128–3137, 2009.
[50]  O. Petrenko, G. Fingerle-Rowson, T. Peng, R. A. Mitchell, and C. N. Metz, “Macrophage migration inhibitory factor deficiency is associated with altered cell growth and reduced susceptibility to Ras-mediated transformation,” The Journal of Biological Chemistry, vol. 278, no. 13, pp. 11078–11085, 2003.
[51]  J. Nishihira, T. Ishibashi, T. Fukushima, B. Sun, Y. Sato, and S. Todo, “Macrophage migration inhibitory factor (MIF): Its potential role in tumor growth and tumor-associated angiogenesis,” Annals of the New York Academy of Sciences, vol. 995, pp. 171–182, 2003.
[52]  B. Bianco, G. M. André, F. L. Vilarino et al., “The possible role of genetic variants in autoimmune-related genes in the development of endometriosis,” Human Immunology, vol. 73, no. 3, pp. 306–315, 2012.
[53]  S. A. Treloar, J. Wicks, D. R. Nyholt et al., “Genomewide linkage study in 1,176 affected sister pair families identifies a significant susceptibility locus for endometriosis on chromosome 10q26,” American Journal of Human Genetics, vol. 77, no. 3, pp. 365–376, 2005.
[54]  M. N. Singh, H. F. Stringfellow, S. E. Taylor et al., “Elevated expression of CYP1A1 and γ-SYNUCLEIN in human ectopic (ovarian) endometriosis compared with eutopic endometrium,” Molecular Human Reproduction, vol. 14, no. 11, pp. 655–663, 2008.
[55]  C.-H. Wu, C.-Y. Guo, J.-G. Yang et al., “Polymorphisms of dioxin receptor complex components and detoxification-related genes jointly confer susceptibility to advanced-stage endometriosis in the taiwanese han population,” American Journal of Reproductive Immunology, vol. 67, no. 2, pp. 160–168, 2012.
[56]  S. Vichi, E. Medda, A. M. Ingelido et al., “Glutathione transferase polymorphisms and risk of endometriosis associated with polychlorinated biphenyls exposure in Italian women: a gene-environment interaction,” Fertility and Sterility, vol. 97, no. 5, pp. 1143.e3–1151.e3, 2012.
[57]  J. N. Painter, D. R. Nyholt, A. Morris et al., “High-density fine-mapping of a chromosome 10q26 linkage peak suggests association between endometriosis and variants close to CYP2C19,” Fertility and Sterility, vol. 95, no. 7, pp. 2236–2240, 2011.
[58]  I. R. Costa, R. C. P. C. Silva, A. B. Frare et al., “Polymorphism of the progesterone receptor gene associated with endometriosis in patients from Goiás, Brazil,” Genetics and Molecular Research, vol. 10, no. 3, pp. 1364–1370, 2011.
[59]  S. Govatati, N. K. Tangudu, M. Deenadayal, B. Chakravarty, S. Shivaji, and M. Bhanoori, “Association of E-cadherin single nucleotide polymorphisms with the increased risk of endometriosis in Indian women,” Molecular Human Reproduction, vol. 18, no. 5, pp. 280–287, 2012.
[60]  S.-W. Guo, “Association of endometriosis risk and genetic polymorphisms involving sex steroid biosynthesis and their receptors: a meta-analysis,” Gynecologic and Obstetric Investigation, vol. 61, no. 2, pp. 90–105, 2006.
[61]  H. Kim, J. H. Park, S.-Y. Ku, S. H. Kim, Y. M. Choi, and J. G. Kim, “Association between endometriosis and polymorphisms in insulin-like growth factors (IGFs) and IGF-I receptor genes in Korean women,” European Journal of Obstetrics Gynecology and Reproductive Biology, vol. 156, no. 1, pp. 87–90, 2011.
[62]  H. Kim, S.-Y. Ku, S. H. Kim, Y. M. Choi, and J. G. Kim, “Association between endometriosis and polymorphisms in insulin-like growth factor binding protein genes in Korean women,” European Journal of Obstetrics Gynecology and Reproductive Biology, vol. 162, no. 1, pp. 96–101, 2012.
[63]  F. ?ayan, D. Ertun, N. Aras-Ate? et al., “Association of G1057D variant of insulin receptor substrate-2 with endometriosis,” Fertility and Sterility, vol. 94, no. 5, pp. 1622–1626, 2010.
[64]  M. Ammendola, N. Bottini, A. Pietropolli, P. Saccucci, and F. Gloria-Bottini, “Association between PTPN22 and endometriosis,” Fertility and Sterility, vol. 89, no. 4, pp. 993–994, 2008.
[65]  G. H. Lee, Y. M. Choi, S. H. Kim et al., “Interleukin-2 receptor β gene C627T polymorphism in Korean women with endometriosis: a case-control study,” Human Reproduction, vol. 24, no. 10, pp. 2596–2599, 2009.
[66]  R. P. Gon?alves-Filho, A. Brandes, D. M. Christofolini, T. G. Lerner, B. Bianco, and C. P. Barbosa, “Plasminogen activator inhibitor-1 4G/5G polymorphism in infertile women with and without endometriosis,” Acta Obstetricia et Gynecologica Scandinavica, vol. 90, no. 5, pp. 473–477, 2011.
[67]  G. M. André, C. P. Barbosa, J. S. Teles, F. L. Vilarino, D. M. Christofolini, and B. Bianco, “Analysis of FOXP3 polymorphisms in infertile women with and without endometriosis,” Fertility and Sterility, vol. 95, no. 7, pp. 2223–2227, 2011.
[68]  C. P. Barbosa, J. S. Teles, T. G. Lerner et al., “Genetic association study of polymorphisms FOXP3 and FCRL3 in women with endometriosis,” Fertility and Sterility, vol. 97, no. 5, pp. 1124–1128, 2012.
[69]  L. A. Ruiz, J. Dutil, A. Ruiz et al., “Single-nucleotide polymorphisms in the lysyl oxidase-like protein 4 and complement component 3 genes are associated with increased risk for endometriosis and endometriosis-associated infertility,” Fertility and Sterility, vol. 96, no. 2, pp. 512–515, 2011.
[70]  F. Medeiros, X. Wang, A. R. C. Araujo et al., “HMGA gene rearrangement is a recurrent somatic alteration in polypoid endometriosis,” Human Pathology, vol. 43, no. 8, pp. 1243–1248, 2012.
[71]  D. R. Nyholt, S. K. Low, C. A. Anderson, et al., “Genome-wide association meta-analysis identifies new endometriosis risk loci,” Nature Genetics, vol. 44, no. 12, pp. 1355–1359, 2012.
[72]  Y. Osuga, K. Koga, Y. Hirota, T. Hirata, O. Yoshino, and Y. Taketani, “Lymphocytes in endometriosis,” American Journal of Reproductive Immunology, vol. 65, no. 1, pp. 1–10, 2011.
[73]  E. Sturlese, F. M. Salmeri, G. Retto et al., “Dysregulation of the Fas/FasL system in mononuclear cells recovered from peritoneal fluid of women with endometriosis,” Journal of Reproductive Immunology, vol. 92, no. 1-2, pp. 74–81, 2011.
[74]  A. S. Laganà, A. D’Ascola, F. M. Salmeri et al., “mRNA expression of Foxp3 and RORc transcription factors and of IL-10 and IL-17A cytokines in ovarian endometrioma of women with endometriosis,” Journal of Endometriosis, vol. 4, no. 4, pp. 227–228, 2012.
[75]  A. S. Laganà, A. Pizzo, A. D’Ascola, et al., “mRNA expression of transcription factors and cytokines in immune cells of ovarian endometrioma from women with endometriosis,” Reproductive Sciences, vol. 20, no. 3, supplement, pp. 146–147, 2013.
[76]  E. Kalu, N. Sumar, T. Giannopoulos et al., “Cytokine profiles in serum and peritoneal fluid from infertile women with and without endometriosis,” Journal of Obstetrics and Gynaecology Research, vol. 33, no. 4, pp. 490–495, 2007.
[77]  L. Zhou, M. M. W. Chong, and D. R. Littman, “Plasticity of CD4+ T Cell Lineage Differentiation,” Immunity, vol. 30, no. 5, pp. 646–655, 2009.
[78]  P. Basta, M. Majka, W. Jozwicki et al., “The frequency of CD25+CD4+ and FOXP3+ regulatory T cells in ectopic endometrium and ectopic decidua,” Reproductive Biology and Endocrinology, vol. 8, article 116, 2010.
[79]  M. J. Polanczyk, C. Hopke, A. A. Vandenbark, and H. Offner, “Treg suppressive activity involves estrogen-dependent expression of programmed death-1 (PD-1),” International Immunology, vol. 19, no. 3, pp. 337–343, 2007.
[80]  M. Berbic and I. S. Fraser, “Regulatory T cells and other leukocytes in the pathogenesis of endometriosis,” Journal of Reproductive Immunology, vol. 88, no. 2, pp. 149–155, 2011.
[81]  T. Hirata, Y. Osuga, K. Hamasaki et al., “Interleukin (IL)-17A stimulates IL-8 secretion, cyclooxygensase-2 expression, and cell proliferation of endometriotic stromal cells,” Endocrinology, vol. 149, no. 3, pp. 1260–1267, 2008.
[82]  T. Hirata, Y. Osuga, M. Takamura et al., “Recruitment of CCR6-expressing Th17 cells by CCL 20 secreted from IL-1β-, TNF-α-, and IL-17A-stimulated endometriotic stromal cells,” Endocrinology, vol. 151, no. 11, pp. 5468–5476, 2010.
[83]  R. A. Budiu, I. Diaconu, R. Chrissluis, A. Dricu, R. P. Edwards, and A. M. Vlad, “A conditional mouse model for human MUC1-positive endometriosis shows the presence of anti-MUC1 antibodies and Foxp3+ regulatory T cells,” Disease Models and Mechanisms, vol. 2, no. 11-12, pp. 593–603, 2009.
[84]  S. Podgaec, L. V. Rizzo, L. F. Fernandes, E. C. Baracat, and M. S. Abrao, “CD4(+) CD25(high) Foxp3(+) cells increased in the peritoneal fluid of patients with endometriosis,” American Journal of Reproductive Immunology, vol. 68, no. 4, pp. 301–308, 2012.
[85]  D. J. Oosterlynck, F. J. Cornillie, M. Waer, M. Vandeputte, and P. R. Koninckx, “Women with endometriosis show a defect in natural killer activity resulting in a decreased cytotoxicity to autologous endometrium,” Fertility and Sterility, vol. 56, no. 1, pp. 45–51, 1991.
[86]  J. Sikora, A. Mielczarek-Palacz, and Z. Kondera-Anasz, “Role of Natural Killer cell activity in the pathogenesis of endometriosis,” Current Medicinal Chemistry, vol. 18, no. 2, pp. 200–208, 2011.
[87]  A. Agic, S. Djalali, K. Diedrich, and D. Hornung, “Apoptosis in endometriosis,” Gynecologic and Obstetric Investigation, vol. 68, no. 4, pp. 217–223, 2009.
[88]  T. Harada, F. Taniguchi, M. Izawa et al., “Apoptosis and endometriosis,” Frontiers in Bioscience, vol. 12, no. 8, pp. 3140–3151, 2007.
[89]  M. Ulukus and A. Arici, “Immunology of endometriosis,” Minerva Ginecologica, vol. 57, no. 3, pp. 237–248, 2005.
[90]  C. D. Gregory and J. D. Pound, “Microenvironmental influences of apoptosis in vivo and in vitro,” Apoptosis, vol. 15, no. 9, pp. 1029–1049, 2010.
[91]  F. Tzifi, C. Economopoulou, D. Gourgiotis, A. Ardavanis, S. Papageorgiou, and A. Scorilas, “The role of BCL2 family of apoptosis regulator proteins in acute and chronic leukemias,” Advances in Hematology, vol. 2012, Article ID 524308, 15 pages, 2012.
[92]  M. E. Peter, R. C. Budd, J. Desbarats et al., “The CD95 receptor: apoptosis revisited,” Cell, vol. 129, no. 3, pp. 447–450, 2007.
[93]  A. Strasser, P. J. Jost, and S. Nagata, “The many roles of FAS receptor signaling in the immune system,” Immunity, vol. 30, no. 2, pp. 180–192, 2009.
[94]  M. Lettau, M. Paulsen, D. Kabelitz, and O. Janssen, “FasL expression and reverse signalling,” Results and Problems in Cell Differentiation, vol. 49, pp. 49–61, 2009.
[95]  T. Suda, T. Takahashi, P. Golstein, and S. Nagata, “Molecular cloning and expression of the Fas ligand, a novel member of the tumor necrosis factor family,” Cell, vol. 75, no. 6, pp. 1169–1178, 1993.
[96]  M. Lettau, M. Paulsen, D. Kabelitz, and O. Janssen, “Storage, expression and function of Fas ligand, the key death factor of immune cells,” Current Medicinal Chemistry, vol. 15, no. 17, pp. 1684–1696, 2008.
[97]  L. A. O Reilly, L. Tai, L. Lee et al., “Membrane-bound Fas ligand only is essential for Fas-induced apoptosis,” Nature, vol. 461, no. 7264, pp. 659–663, 2009.
[98]  A. Paunel-G?rgülü, S. Flohé, M. Scholz, J. Windolf, and T. L?gters, “Increased serum soluble Fas after major trauma is associated with delayed neutrophil apoptosis and development of sepsis,” Critical Care, vol. 15, no. 1, p. R20, 2011.
[99]  R. Weinlich, T. Brunner, and G. P. Amarante-Mendes, “Control of death receptor ligand activity by posttranslational modifications,” Cellular and Molecular Life Sciences, vol. 67, no. 10, pp. 1631–1642, 2010.
[100]  L. Cabal-Hierro and P. S. Lazo, “Signal transduction by tumor necrosis factor receptors,” Cellular Signalling, vol. 24, no. 6, pp. 1297–1305, 2012.
[101]  A. S. Laganà, F. M. Salmeri, G. Retto et al., “Stage-related changes of peritoneal soluble TNFαand TNFR1 and TNFR2 in cells recovered from PF of women with endometriosis,” Journal of Reproductive Immunology, vol. 94, no. 1, pp. 94–95, 2012.
[102]  Z. Z. Zhao, D. R. Nyholt, L. Le et al., “Genetic variation in tumour necrosis factor and lymphotoxin is not associated with endometriosis in an Australian sample,” Human Reproduction, vol. 22, no. 9, pp. 2389–2397, 2007.
[103]  S. J. Chae, H. Kim, B. C. Jee, C. S. Suh, S. H. Kim, and J. G. Kim, “Tumor necrosis factor (TNF)-TNF receptor gene polymorphisms and their serum levels in Korean women with endometriosis,” American Journal of Reproductive Immunology, vol. 60, no. 5, pp. 432–439, 2008.
[104]  K. Vijaya Lakshmi, P. Shetty, K. Vottam, S. Govindhan, S. N. Ahmad, and Q. Hasan, “Tumor necrosis factor alpha -C850T polymorphism is significantly associated with endometriosis in Asian Indian women,” Fertility and Sterility, vol. 94, no. 2, pp. 453–456, 2010.
[105]  W. Paul Dmowski and D. P. Braun, “Immunology of endometriosis,” Best Practice & Research Clinical Obstetrics & Gynaecology, vol. 18, no. 2, pp. 245–263, 2004.
[106]  A. B. Trovó de Marqui, “Genetic polymorphisms and endometriosis: contribution of genes that regulate vascular function and tissue remodeling,” Revista da Associa??o Médica Brasileira, vol. 58, no. 5, pp. 620–632, 2012.
[107]  K. Khoufache, P. K. Bondza, N. Harir, et al., “Soluble human IL-1 receptor type 2 inhibits ectopic endometrial tissue implantation and growth: identification of a novel potential target for endometriosis treatment,” The American Journal of Pathology, vol. 181, no. 4, pp. 1197–1205, 2012.
[108]  J. Sikora, A. Mielczarek-Palacz, and Z. Kondera-Anasz, “Imbalance in cytokines from interleukin-1 family—role in pathogenesis of endometriosis,” American Journal of Reproductive Immunology, vol. 68, no. 2, pp. 138–45, 2012.
[109]  N. A. Bersinger, H. Dechaud, B. McKinnon, and M. D. Mueller, “Analysis of cytokinesin the peritoneal fluid of endometriosispatients as a function of the menstrual cycle stage using the Bio-Plex platform,” Archives of Physiology and Biochemistry, vol. 118, no. 4, pp. 210–218, 2012.
[110]  D. Wickiewicz, A. Chrobak, G. B. Gmyrek et al., “Diagnostic accuracy of interleukin-6 levels in peritoneal fluid for detection of endometriosis,” Archives of Gynecology and Obstetrics, 2013.
[111]  F. Carmona, C. Chapron, M. á. Martínez-Zamora, et al., “Ovarian endometrioma but not deep infiltrating endometriosis is associated with increased serum levels of interleukin-8 and interleukin-6,” Journal of Reproductive Immunology, vol. 95, no. 1-2, pp. 80–86, 2012.
[112]  W. Fan, S. Li, Q. Chen, Z. Huang, Q. Ma, and Z. Xiao, “Association between interleukin-10 promoter polymorphisms and endometriosis: a meta-analysis,” Gene, vol. 515, no. 1, pp. 49–55, 2013.
[113]  A. Arici, I. Matalliotakis, A. Goumenou et al., “Increased levels of interleukin-15 in the peritoneal fluid of women with endometriosis: inverse correlation with stage and depth of invasion,” Human Reproduction, vol. 18, no. 2, pp. 429–432, 2003.
[114]  F. Zhang, Y. Yang, and Y. Wang, “Association between TGF-β1-509C/T polymorphism and endometriosis: a systematic review and meta-analysis,” European Journal of Obstetrics & Gynecology and Reproductive Biology, vol. 164, no. 2, pp. 121–126, 2012.
[115]  A. Arici, I. Matalliotakis, A. Goumenou, G. Koumantakis, S. Vassiliadis, and N. G. Mahutte, “Altered expression of interleukin-18 in the peritoneal fluid of women with endometriosis,” Fertility and Sterility, vol. 80, no. 4, pp. 889–894, 2003.
[116]  P. Santulli, B. Borghese, S. Chouzenoux, et al., “Interleukin-19 and interleukin-22 serum levels are decreased in patients with ovarian endometrioma,” Fertility and Sterility, vol. 99, no. 1, pp. 219–226, 2013.
[117]  P. Santulli, B. Borghese, S. Chouzenoux, et al., “Serum and peritoneal interleukin-33 levels are elevated in deeply infiltrating endometriosis,” Human Reproduction, vol. 27, no. 7, pp. 2001–2009, 2012.
[118]  M. Y. Wu and H. N. Ho, “The role of cytokines in endometriosis,” American Journal of Reproductive Immunology, vol. 49, no. 5, pp. 285–296, 2003.
[119]  T. M. D'Hooghe, N. P. Nugent, S. Cuneo et al., “Recombinant human TNFRSF1A (r-hTBP1) inhibits the development of endometriosis in baboons: a prospective, randomized, placebo- and drug-controlled study,” Biology of Reproduction, vol. 74, no. 1, pp. 131–136, 2006.
[120]  H. Falconer, J. M. Mwenda, D. C. Chai et al., “Treatment with anti-TNF monoclonal antibody (c5N) reduces the extent of induced endometriosis in the baboon,” Human Reproduction, vol. 21, no. 7, pp. 1856–1862, 2006.
[121]  T. Harada, A. Enatsu, M. Mitsunari et al., “Role of cytokines in progression of endometriosis,” Gynecologic and Obstetric Investigation, vol. 47, supplement 1, pp. 34–40, 1999.
[122]  A. G. Braundmeier and R. A. Nowak, “Cytokines regulate matrix metalloproteinases in human uterine endometrial fibroblast cells through a mechanism that does not involve increases in extracellular matrix metalloproteinase inducer,” American Journal of Reproductive Immunology, vol. 56, no. 3, pp. 201–214, 2006.
[123]  K. L. Bruner-Tran, E. Eisenberg, G. R. Yeaman, T. A. Anderson, J. McBean, and K. G. Osteen, “Steroid and cytokine regulation of matrix metalloproteinase expression in endometriosis and the establishment of experimental endometriosis in nude mice,” Journal of Clinical Endocrinology and Metabolism, vol. 87, no. 10, pp. 4782–4791, 2002.
[124]  J. Donnez, P. Smoes, S. Gillerot, F. Casanas-Roux, and M. Nisolle, “Vascular endothelial growth factor (VEGF) in endometriosis,” Human Reproduction, vol. 13, no. 6, pp. 1686–1690, 1998.
[125]  A. Fasciani, G. D'Ambrogio, G. Bocci, M. Monti, A. R. Genazzani, and P. G. Artini, “High concentrations of the vascular endothelial growth factor and interleukin-8 in ovarian endometriomata,” Molecular Human Reproduction, vol. 6, no. 1, pp. 50–54, 2000.
[126]  J. McLaren, A. Prentice, D. S. Charnock-Jones, and S. K. Smith, “Vascular endothelial growth factor (VEGF) concentrations are elevated in peritoneal fluid of women with endometriosis,” Human Reproduction, vol. 11, no. 1, pp. 220–223, 1996.
[127]  M. Takehara, M. Ueda, Y. Yamashita, Y. Terai, Y.-C. Hung, and M. Ueki, “Vascular endothelial growth factor A and C gene expression in endometriosis,” Human Pathology, vol. 35, no. 11, pp. 1369–1375, 2004.
[128]  J. E. Girling and P. A. W. Rogers, “Recent advances in endometrial angiogenesis research,” Angiogenesis, vol. 8, no. 2, pp. 89–99, 2005.
[129]  J. Gilabert-Estellés, L. A. Ramón, F. Espa?a et al., “Expression of angiogenic factors in endometriosis: relationship to fibrinolytic and metalloproteinase systems,” Human Reproduction, vol. 22, no. 8, pp. 2120–2127, 2007.
[130]  A. Braza-Bo?ls, J. Gilabert-Estellés, L. A. Ramón et al., “Peritoneal fluid reduces angiogenesis-related MicroRNA expression in cell cultures of endometrial and endometriotic tissues from women with endometriosis,” PLoS One, vol. 8, no. 4, Article ID e62370, 2013.
[131]  E. Barcz, ?. Milewski, P. Dziunycz, P. Kamiński, R. P?oski, and J. Malejczyk, “Peritoneal cytokines and adhesion formation in endometriosis: an inverse association with vascular endothelial growth factor concentration,” Fertility and Sterility, vol. 97, no. 6, pp. 1380.e1–1386.e1, 2012.
[132]  R. Cosín, J. Gilabert-Estellés, L. A. Ramón et al., “Vascular endothelial growth factor polymorphisms (-460C/T, +405G/C, and 936C/T) and endometriosis: their influence on vascular endothelial growth factor expression,” Fertility and Sterility, vol. 92, no. 4, pp. 1214–1220, 2009.
[133]  B. Emamifar, Z. Salehi, M. Mehrafza, and F. Mashayekhi, “The vascular endothelial growth factor (VEGF) polymorphisms and the risk of endometriosis in northern Iran,” Gynecological Endocrinology, vol. 28, no. 6, pp. 447–450, 2012.
[134]  J.-H. Kim, Y.-I. Yang, J.-H. Ahn, J.-G. Lee, K.-T. Lee, and J.-H. Choi, “Deer (Cervus elaphus) antler extract suppresses adhesion and migration of endometriotic cells and regulates MMP-2 and MMP-9 expression,” Journal of Ethnopharmacology, vol. 140, no. 2, pp. 391–397, 2012.
[135]  K. G. Osteen, G. R. Yeaman, and K. L. Bruner-Tran, “Matrix metalloproteinases and endometriosis,” Seminars in Reproductive Medicine, vol. 21, no. 2, pp. 155–164, 2003.
[136]  R. Shaco-Levy, S. Sharabi, B. Piura, and N. Sion-Vardy, “MMP-2, TIMP-1, E-cadherin, and β;-catenin expression in endometrial serous carcinoma compared with low-grade endometrial endometrioid carcinoma and proliferative endometrium,” Acta Obstetricia et Gynecologica Scandinavica, vol. 87, no. 8, pp. 868–874, 2008.
[137]  K.-H. Kim, E. N. Lee, J. K. Park et al., “Curcumin attenuates TNF-α-induced expression of intercellular adhesion molecule-1, vascular cell adhesion molecule-1 and proinflammatory cytokines in human endometriotic stromal cells,” Phytotherapy Research, vol. 26, no. 7, pp. 1037–1047, 2012.
[138]  M. Berkkanoglu and A. Arici, “Immunology and endometriosis,” American Journal of Reproductive Immunology, vol. 50, no. 1, pp. 48–59, 2003.
[139]  P. Vigano, B. Magri, M. Busacca, M. Vignali, R. Pardi, and A. M. Di Blasio, “Expression of intercellular adhesion molecule-1 (ICAM-1) on cultured human endometrial stromal cells and its role in the interaction with natural killers,” American Journal of Reproductive Immunology, vol. 32, no. 3, pp. 139–145, 1994.
[140]  S. Defrère, J. Donnez, P. Moulin et al., “Expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 in human endometrial stromal and epithelial cells is regulated by interferon-gamma but not iron,” Gynecologic and Obstetric Investigation, vol. 65, no. 3, pp. 145–154, 2008.
[141]  P. Viganò, E. Somigliana, B. Gaffuri, R. Santorsola, M. Busacca, and M. Vignali, “Endometrial release of soluble intercellular adhesion molecule 1 and endometriosis: relationship to the extent of the disease,” Obstetrics and Gynecology, vol. 95, no. 1, pp. 115–118, 2000.
[142]  C. M. Kyama, L. Overbergh, A. Mihalyi et al., “Endometrial and peritoneal expression of aromatase, cytokines, and adhesion factors in women with endometriosis,” Fertility and Sterility, vol. 89, no. 2, pp. 301–310, 2008.
[143]  M. H. Wu, P. C. Chuang, Y. J. Lin, and S. J. Tsai, “Suppression of annexin A2 by prostaglandin E2 impairs phagocytic ability of peritoneal macrophages in women with endometriosis,” Human Reproduction, vol. 28, no. 4, pp. 1045–1053, 2013.
[144]  H. Maia Jr., C. Haddad, G. Coelho, and J. Casoy, “Role of inflammation and aromatase expression in the eutopic endometrium and its relationship with the development of endometriosis,” Womens Health, vol. 8, no. 6, pp. 647–658, 2012.
[145]  S. E. Bulun, Y.-H. Cheng, M. E. Pavone et al., “17β-Hydroxysteroid dehydrogenase-2 deficiency and progesterone resistance in endometriosis,” Seminars in Reproductive Medicine, vol. 28, no. 1, pp. 44–50, 2010.
[146]  Y.-H. Cheng, A. Imir, V. Fenkci, M. B. Yilmaz, and S. E. Bulun, “Stromal cells of endometriosis fail to produce paracrine factors that induce epithelial 17β-hydroxysteroid dehydrogenase type 2 gene and its transcriptional regulator Sp1: a mechanism for defective estradiol metabolism,” American Journal of Obstetrics and Gynecology, vol. 196, no. 4, pp. 391.e1–398.e1, 2007.
[147]  F. Machado-Linde, P. Pelegrin, M. L. Sanchez-Ferrer, J. Leon, P. Cascales, and J. J. Parrilla, “2-methoxyestradiol in the pathophysiology of endometriosis: focus on angiogenesis and therapeutic potential,” Reproductive Sciences, vol. 19, no. 10, pp. 1018–1029, 2012.
[148]  S. A. Missmer, S. E. Hankinson, D. Spiegelman et al., “Reproductive history and endometriosis among premenopausal women,” Obstetrics and Gynecology, vol. 104, no. 5, pp. 965–974, 2004.
[149]  J. Cumiskey, P. Whyte, P. Kelehan, and D. Gibbons, “A detailed morphologic and immunohistochemical comparison of pre- and postmenopausal endometriosis,” Journal of Clinical Pathology, vol. 61, no. 4, pp. 455–459, 2008.
[150]  C. Parente Barbosa, A. M. Bentes De Souza, B. Bianco, and D. M. Christofolini, “The effect of hormones on endometriosis development,” Minerva Ginecologica, vol. 63, no. 4, pp. 375–386, 2011.
[151]  J. M. P. Pabona, F. A. Simmen, M. A. Nikiforov et al., “Krüppel-like factor 9 and progesterone receptor coregulation of decidualizing endometrial stromal cells: implications for the pathogenesis of endometriosis,” Journal of Clinical Endocrinology and Metabolism, vol. 97, no. 3, pp. E376–E392, 2012.
[152]  D. Vinatier, G. Orazi, M. Cosson, and P. Dufour, “Theories of endometriosis,” European Journal of Obstetrics Gynecology and Reproductive Biology, vol. 96, no. 1, pp. 21–34, 2001.
[153]  S. S. Andrade, A. D. Azevedo, I. C. Monasterio, et al., “17β-Estradiol and steady-state concentrations of H2O2: antiapoptotic effect in endometrial cells from patients with endometriosis,” Free Radical Biology & Medicine, vol. 60, pp. 63–72, 2013.
[154]  W. Di and S. W. Guo, “The search for genetic variants predisposing women to endometriosis,” Current Opinion in Obstetrics and Gynecology, vol. 19, no. 4, pp. 395–401, 2007.
[155]  W. Fan, S. Li, Q. Chen, Z. Huang, Q. Ma, and Z. Xiao, “Association between interleukin-10 promoter polymorphisms and endometriosis: a meta-analysis,” Gene, vol. 515, no. 1, pp. 49–55, 2013.
[156]  K. Kashima, T. Ishimaru, H. Okamura et al., “Familial risk among Japanese patients with endometriosis,” International Journal of Gynecology and Obstetrics, vol. 84, no. 1, pp. 61–64, 2004.
[157]  S. Kennedy, H. Mardon, and D. Barlow, “Familial endometriosis,” Journal of Assisted Reproduction and Genetics, vol. 12, no. 1, pp. 32–34, 1995.
[158]  J. N. Hirschhorn, K. Lohmueller, E. Byrne, and K. Hirschhorn, “A comprehensive review of genetic association studies,” Genetics in Medicine, vol. 4, no. 2, pp. 45–61, 2002.
[159]  C. A. McCarty, R. L. Berg, J. D. Welter, T. E. Kitchner, and J. W. Kemnitz, “A novel gene-environment interaction involved in endometriosis,” International Journal of Gynecology and Obstetrics, vol. 116, no. 1, pp. 61–63, 2012.
[160]  M. Ballester, P. Dehan, A. Béliard, G. Brichant, and M. Nisolle, “Role of genetic and environmental factors in the development of endometriosis,” Revue Médicale de Liège, vol. 67, no. 5-6, pp. 374–380, 2012.
[161]  N. Rahmioglu, S. A. Missmer, G. W. Montgomery, and K. T. Zondervan, “Insights into assessing the genetics of endometriosis,” Current Obstetrics and Gynecology Reports, vol. 1, no. 3, pp. 124–137, 2012.
[162]  H. Falconer, T. D'Hooghe, and G. Fried, “Endometriosis and genetic polymorphisms,” Obstetrical and Gynecological Survey, vol. 62, no. 9, pp. 616–628, 2007.
[163]  X. Zhao, L.-L. Zong, Y.-F. Wang et al., “Association of single nucleotide polymorphism in CYP17 and ERα genes with endometriosis risk in southern Chinese women,” Zhonghua Yi Xue Yi Chuan Xue Za Zhi, vol. 28, no. 3, pp. 304–307, 2011.
[164]  S. Vainio, M. Heikkil?, A. Kispert, N. Chin, and A. P. McMahon, “Female development in mammals is regulated by Wnt-4 signalling,” Nature, vol. 397, no. 6718, pp. 405–409, 1999.
[165]  X. Guo, C. Jing, L. Li et al., “Down-regulation of VEZT gene expression in human gastric cancer involves promoter methylation and miR-43c,” Biochemical and Biophysical Research Communications, vol. 404, no. 2, pp. 622–627, 2011.
[166]  A. Boyer, é. Lapointe, X. Zheng et al., “WNT4 is required for normal ovarian follicle development and female fertility,” FASEB Journal, vol. 24, no. 8, pp. 3010–3025, 2010.
[167]  J. M. Rae, M. D. Johnson, J. O. Scheys, K. E. Cordero, J. M. Larios, and M. E. Lippman, “GREB1 is a critical regulator of hormone dependent breast cancer growth,” Breast Cancer Research and Treatment, vol. 92, no. 2, pp. 141–149, 2005.
[168]  P. Acién, M. Acién, and M. Sánchez-Ferrer, “Complex malformations of the female genital tract. New types and revision of classification,” Human Reproduction, vol. 19, no. 10, pp. 2377–2384, 2004.
[169]  K. Morcel, D. Guerrier, T. Watrin, I. Pellerin, and J. Levêque, “The Mayer-Rokitansky-Küster-Hauser (MRKH) syndrome: clinical description and genetics,” Journal de Gynecologie Obstetrique et Biologie de la Reproduction, vol. 37, no. 6, pp. 539–546, 2008.
[170]  A. Zanatta, A. M. Rocha, F. M. Carvalho et al., “The role of the Hoxa10/HOXA10 gene in the etiology of endometriosis and its related infertility: a review,” Journal of Assisted Reproduction and Genetics, vol. 27, no. 12, pp. 701–710, 2010.
[171]  R. Krumlauf, “Hox genes in vertebrate development,” Cell, vol. 78, no. 2, pp. 191–201, 1994.
[172]  H. S. Taylor, G. B. Vanden Heuvel, and P. Igarashi, “A conserved Hox axis in the mouse and human female reproductive system: late establishment and persistent adult expression of the Hoxa cluster genes,” Biology of Reproduction, vol. 57, no. 6, pp. 1338–1345, 1997.
[173]  D. Modi and G. Godbole, “HOXA10 signals on the highway through pregnancy,” Journal of Reproductive Immunology, vol. 83, no. 1-2, pp. 72–78, 2009.
[174]  H. Lim, L. Ma, W.-G. Ma, R. L. Maas, and S. K. Dey, “Hoxa-10 regulates uterine stromal cell responsiveness to progesterone during implantation and decidualization in the mouse,” Molecular Endocrinology, vol. 13, no. 6, pp. 1005–1017, 1999.
[175]  J. N. Painter, C. A. Anderson, D. R. Nyholt et al., “Genome-wide association study identifies a locus at 7p15.2 associated with endometriosis,” Nature Genetics, vol. 43, no. 1, pp. 51–54, 2011.
[176]  W. Cheng, J. Liu, H. Yoshida, D. Rosen, and H. Naora, “Lineage infidelity of epithelial ovarian cancers is controlled by HOX genes that specify regional identity in the reproductive tract,” Nature Medicine, vol. 11, no. 5, pp. 531–537, 2005.
[177]  B. Borghese, D. Vaiman, D. de Ziegler, and C. Chapron, “Endometriosis and genetics: what responsibility for the genes?” Journal de Gynecologie Obstetrique et Biologie de la Reproduction, vol. 39, no. 3, pp. 196–207, 2010.
[178]  G. S. Daftary and H. S. Taylor, “EMX2 gene expression in the female reproductive tract and aberrant expression in the endometrium of patients with endometriosis,” Journal of Clinical Endocrinology and Metabolism, vol. 89, no. 5, pp. 2390–2396, 2004.
[179]  J. Lin, L. Zong, S. H. Kennedy, and K. T. Zondervan, “Coding regions of INHBA, SFRP4 and HOXA10 are not implicated in familial endometriosis linked to chromosome 7p13-15,” Molecular Human Reproduction, vol. 17, no. 10, pp. 605–611, 2011.
[180]  A. Biason-Lauber, D. Konrad, F. Navratil, and E. J. Schoenle, “A WNT4 mutation associated with Müllerian-Duct regression and virilization in a 46,XX woman,” The New England Journal of Medicine, vol. 351, no. 8, pp. 792–798, 2004.
[181]  A. Biason-Lauber, G. De Filippo, D. Konrad, G. Scarano, A. Nazzaro, and E. J. Schoenle, “WNT4 deficiency-a clinical phenotype distinct from the classic Mayer-Rokitansky-Kuster-Hauser syndrome: a case report,” Human Reproduction, vol. 22, no. 1, pp. 224–229, 2007.
[182]  K. Hayashi, D. W. Erikson, S. A. Tilford et al., “Wnt genes in the mouse uterus: potential regulation of implantation,” Biology of Reproduction, vol. 80, no. 5, pp. 989–1000, 2009.
[183]  S. Sonderegger, J. Pollheimer, and M. Kn?fler, “Wnt signalling in implantation, decidualisation and placental differentiation—review,” Placenta, vol. 31, no. 10, pp. 839–847, 2010.
[184]  S. Matsuzaki, C. Darcha, E. Maleysson, M. Canis, and G. Mage, “Impaired down-regulation of E-cadherin and β-catenin protein expression in endometrial epithelial cells in the mid-secretory endometrium of infertile patients with endometriosis,” Journal of Clinical Endocrinology and Metabolism, vol. 95, no. 7, pp. 3437–3445, 2010.
[185]  S. Bondos, “Variations on a theme: Hox and Wnt combinatorial regulation during animal development,” Science's STKE, vol. 2006, no. 355, p. pe38, 2006.
[186]  Z. Klapholz-Brown, G. G. Walmsley, Y. M. Nusse, R. Nusse, and P. O. Brown, “Transcriptional program induced by Wnt protein in human fibroblasts suggests mechanisms for cell cooperativity in defining tissue microenvironments,” PLoS One, vol. 2, no. 9, article e945, 2007.
[187]  J. Deschamps, “Ancestral and recently recruited global control of the Hox genes in development,” Current Opinion in Genetics and Development, vol. 17, no. 5, pp. 422–427, 2007.
[188]  I. Cervelló, C. Gil-Sanchis, A. Mas et al., “Human endometrial side population cells exhibit genotypic, phenotypic and functional features of somatic stem cells,” PLoS One, vol. 5, no. 6, Article ID e10964, 2010.
[189]  S. Tsuji, M. Yoshimoto, K. Takahashi, Y. Noda, T. Nakahata, and T. Heike, “Side population cells contribute to the genesis of human endometrium,” Fertility and Sterility, vol. 90, no. 4, supplement, pp. 1528–1537, 2008.
[190]  A. Bratincsák, M. J. Brownstein, R. Cassiani-Ingoni et al., “CD45-positive blood cells give rise to uterine epithelial cells in mice,” Stem Cells, vol. 25, no. 11, pp. 2820–2826, 2007.
[191]  H. Masuda, Y. Matsuzaki, E. Hiratsu et al., “Stem cell-like properties of the endometrial side population: implication in endometrial regeneration,” PLoS One, vol. 5, no. 4, Article ID e10387, 2010.
[192]  L. Ye, R. Mayberry, C. Y. Lo et al., “Generation of human female reproductive tract epithelium from human embryonic stem cells,” PLoS One, vol. 6, no. 6, Article ID e21136, 2011.
[193]  K. E. Schwab, R. W. S. Chan, and C. E. Gargett, “Putative stem cell activity of human endometrial epithelial and stromal cells during the menstrual cycle,” Fertility and Sterility, vol. 84, supplement 2, pp. 1124–1130, 2005.
[194]  T. Ikoma, S. Kyo, Y. Maida et al., “Bone marrow-derived cells from male donors can compose endometrial glands in female transplant recipients,” American Journal of Obstetrics and Gynecology, vol. 201, no. 6, pp. 608.e1–608.e8, 2009.
[195]  H. S. Taylor, “Endometrial cells derived from donor stem cells in bone marrow transplant recipients,” Journal of the American Medical Association, vol. 292, no. 1, pp. 81–85, 2004.
[196]  C. E. Gargett and H. Masuda, “Adult stem cells in the endometrium,” Molecular Human Reproduction, vol. 16, no. 11, pp. 818–834, 2010.
[197]  T. Maruyama, H. Masuda, M. Ono, T. Kajitani, and Y. Yoshimura, “Human uterine stem/progenitor cells: their possible role in uterine physiology and pathology,” Reproduction, vol. 140, no. 1, pp. 11–22, 2010.
[198]  J. A. Sampson, “Peritoneal endometriosis due to menstrual dissemination of endometrial tissue into the peritoneal cavity,” American Journal of Obstetrics & Gynecology, vol. 14, pp. 442–469, 1927.
[199]  K. N. Khan, M. Kitajima, K. Hiraki et al., “Immunopathogenesis of pelvic endometriosis: role of hepatocyte growth factor, macrophages and ovarian steroids,” American Journal of Reproductive Immunology, vol. 60, no. 5, pp. 383–404, 2008.
[200]  P. Bellelis, J. A. Dias Jr., S. Podgaec, M. Gonzales, E. C. Baracat, and M. S. Abr?o, “Epidemiological and clinical aspects of pelvic endometriosis—series of cases,” Revista da Associacao Medica Brasileira, vol. 56, no. 4, pp. 467–471, 2010.
[201]  D. L. Anger and W. G. Foster, “The link between environmental toxicant exposure and endometriosis,” Frontiers in Bioscience, vol. 13, no. 4, pp. 1578–1593, 2008.
[202]  M. Ichida, A. Gomi, N. Hiranouchi et al., “A case of cerebral endometriosis causing catamenial epilepsy,” Neurology, vol. 43, no. 12, pp. 2708–2709, 1993.
[203]  O. Laghzaoui and M. Laghzaoui, “Nasal endometriosis: apropos of 1 case,” Journal de Gynecologie Obstetrique et Biologie de la Reproduction, vol. 30, no. 8, pp. 786–788, 2001.
[204]  V. Barresi, S. Cerasoli, E. Vitarelli, and R. Donati, “Spinal intradural müllerianosis: a case report,” Histology and Histopathology, vol. 21, no. 10–12, pp. 1111–1114, 2006.
[205]  V. Sepilian and C. Della Badia, “Iatrogenic endometriosis caused by uterine morcellation during a supracervical hysterectomy,” Obstetrics and Gynecology, vol. 102, no. 5, pp. 1125–1127, 2003.
[206]  P. G. Signorile, F. Baldi, R. Bussani, M. D'Armiento, M. De Falco, and A. Baldi, “Ectopic endometrium in human foetuses is a common event and sustains the theory of müllerianosis in the pathogenesis of endometriosis, a disease that predisposes to cancer,” Journal of Experimental and Clinical Cancer Research, vol. 28, no. 1, article 49, 2009.
[207]  P. G. Signorile, F. Baldi, R. Bussani et al., “New evidence of the presence of endometriosis in the human fetus,” Reproductive BioMedicine Online, vol. 21, no. 1, pp. 142–147, 2010.
[208]  P. G. Signorile, F. Baldi, R. Bussani et al., “Embryologic origin of endometriosis: analysis of 101 human female fetuses,” Journal of Cellular Physiology, vol. 227, no. 4, pp. 1653–1656, 2012.

Full-Text

comments powered by Disqus

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133

WeChat 1538708413