Endometriosis and Infertility: New Concepts

Ryan, Isabelle P.; Taylor, Robert N.

doi:10.1097/00006254-199911001-00030

Cited by 29 publications

(38 citation statements)

References 46 publications

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“…Thirdly, PGE 2 induces StAR, P450scc, 3 ␤ -HSD-2, P450c17, and aromatase [44] . Fourthly, endometriotic stromal cells are over 100 times more sensitive to IL-1 ␤ stimulation than its eutopic counterpart, resulting in higher COX-2 expression [39] , which induces more local production of PGE 2 [51,52] , and other cytokines are reported to be increased in the peritoneal fluid of women with endometriosis [53] , these cytokines mediate pain, inflammation, and infertility [54] and are a source for maintaining high COX-2 expression, thus perpetuating the positive feedback cycle.…”

Section: Our Current Understanding Of the Pathogenesis Of Endometriosismentioning

confidence: 99%

Nuclear Factor-κB (NF-κB): An Unsuspected Major Culprit in the Pathogenesis of Endometriosis That Is Still at Large?

Guo¹

2006

Gynecol Obstet Invest

125

106

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Endometriosis, defined as the ectopic presence of endometrial glandular and stromal cells outside the uterine cavity, is a common benign gynecological disorder with an enigmatic pathogenesis. Many genes and gene products have been reported to be altered in endometriosis, yet some of them may not be major culprits but merely unwitting accomplices or even innocent bystanders. Therefore, the identification and apprehension of major culprits in the pathogenesis of endometriosis are crucial to the understanding of the pathogenesis and would help to develop better therapeutics for endometriosis. Although so far NF-ĸB only has left few traces of incriminating fingerprints, several lines of investigation suggest that NF-ĸB, a pivotal pro-inflammatory transcription factor, could promote and maintain endometriosis. Various inflammatory agents, growth factors, and oxidative stress activate NF-ĸB. NF-ĸB proteins themselves and proteins regulated by them have been linked to cellular transformation, proliferation, apoptosis, angiogenesis, and invasion. Interestingly, all existing and nearly all investigational medications for endometriosis appear to act through suppression of NF-ĸB activation. In endometriotic cells, NF-ĸB appears to be constitutively activated, and suppression of NF-ĸB activity by NF-ĸB inhibitors or proteasome inhibitors suppresses proliferation in vitro. Viewing NF-ĸB as a major culprit, an autoregulatory loop model can be postulated, which is consistent with existing data and, more importantly, can explain several puzzling phenomena that are otherwise difficult to interpret based on prevailing theories. This view has immediate and important implications for novel ways to treat endometriosis. Further research is warranted to precisely delineate the roles of NF-ĸB in the pathogenesis of endometriosis and to indict and convict its aiders and abettors.

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Section: Our Current Understanding Of the Pathogenesis Of Endometriosismentioning

confidence: 99%

Nuclear Factor-κB (NF-κB): An Unsuspected Major Culprit in the Pathogenesis of Endometriosis That Is Still at Large?

Guo¹

2006

Gynecol Obstet Invest

125

106

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“…The incidence of endometriosis in the general female population ranges from 5% to 15% but can reach 50% in infertile women [28,31,33]. Endometriosis has been tentatively explained on the basis of the metaplasia and transplantation theories [27,29].…”

Section: Introductionmentioning

confidence: 99%

Eutopic endometrium and peritoneal, ovarian and bowel endometriotic tissues express a different profile of matrix metalloproteinases-2, -3 and -11, and of tissue inhibitor metalloproteinases-1 and -2

et al. 2004

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Endometriosis is subsequent to the ability of endometrial glands to invade normal tissues. Matrix metalloproteinases (MMPs)--enzymes that mediate normal tissue turnover, including endometrial breakdown during menstruation-appear to be involved in this invasive process. Here, we examined the immunohistochemical expression of MMP-2, MMP-3, MMP-11, tissue inhibitor metalloproteinase (TIMP)-1 and TIMP-2 in endometrium from women with (n=9) or without endometriosis (n=18) in comparison with peritoneal (n=20), ovarian (n=20) and colorectal endometriosis (n=20). Women with endometriosis showed decreased endometrial MMP-2 expression compared with women without endometriosis (mean+/-SD positive cells: 24.3+/-28.3% and 69.3+/-12.1%), together with loss of MMP-3 expression (0 versus 17.5%+/-20.2). MMP-11, TIMP-1 and TIMP-2 expression was similar in the two groups. Endometrial MMP-2, -3 and -11 expression and TIMP-1 and -2 expression were similar in women with endometriosis and in those with peritoneal endometriosis. MMP-2, -3 and -11 expression was higher in colorectal endometriosis than in ovarian and peritoneal endometriosis. TIMP-2 expression was lower in colorectal endometriosis (P=0.0002) and ovarian endometriotic cysts (P=0.003) than in peritoneal endometriosis. TIMP-1 expression did not vary according to the location of endometriotic lesions. These results suggest that MMP-2 and -3 and TIMP-2 may be involved in the pathogenesis of endometriosis. Interestingly, MMP-2 and -3 overexpression was related to the infiltrative nature of endometriotic lesions, with possible sequential expression from peritoneal to colorectal endometriosis.

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“…The transplantation theory implies that endometrial cells have the ability to detach from the endometrium, reattach after passive transport through the Fallopian tubes into the peritoneum and invade target tissues. The incidence of endometriosis in the general female population ranges from 5% to 15%, but reaches more than 50% in women with dysmenorrhea and/or infertility [34,38,40]. Clinically, one of the most frequent locations of endometriosis has been the ovary, with cysts called endometriomas [18].…”

Section: Introductionmentioning

confidence: 99%

Expression of apoptosis-related proteins in endometriomas and benign and malignant ovarian tumours

et al. 2003

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Apoptosis is a physiological process by which multicellular organisms eliminate superfluous cells. Alterations in apoptosis play a key role in tumour development. The objective was to evaluate the immunohistochemical expression of p53, p21, bax, bak, fas, bcl-2 and bcl-x proteins in 10 endometriomas, 20 benign ovarian tumours (10 mucinous, 10 serous) and 30 malignant ovarian tumours (9 mucinous, 19 serous; 2 endometrioids). p53 positive cells (mean+/-SD) in endometriomas, and benign and malignant tumours were 1.9+/-3.2, 0 and 16.2+/-33.0, respectively. The difference was significant between benign tumours and endometriomas (P=0.003) but not between endometriomas and malignant tumours. P21 expression in endometriomas and benign and malignant tumours was 19.5+/-27.8, 1.7+/-6.7 and 4.1+/-8.6, respectively. Increased p21 expression was found in endometriomas compared with benign (P=0.001) and malignant (P=0.01) tumours. Bax expression was higher in endometriomas than in benign tumours (P=0.01), but no difference was found between endometriomas and malignant tumours. No difference in bak, fas, bcl-2 or bcl-x expression was observed among the groups. In endometriomas, a negative correlation was found between p53 and fas expression (P=0.04, r=0.66). Although endometriomas have histological features of benign ovarian tumours, endometriomas share with malignant ovarian tumours certain alterations in apoptosis-related proteins.

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Endometriosis and Infertility: New Concepts

Cited by 29 publications

References 46 publications

Nuclear Factor-κB (NF-κB): An Unsuspected Major Culprit in the Pathogenesis of Endometriosis That Is Still at Large?

Nuclear Factor-κB (NF-κB): An Unsuspected Major Culprit in the Pathogenesis of Endometriosis That Is Still at Large?

Eutopic endometrium and peritoneal, ovarian and bowel endometriotic tissues express a different profile of matrix metalloproteinases-2, -3 and -11, and of tissue inhibitor metalloproteinases-1 and -2

Expression of apoptosis-related proteins in endometriomas and benign and malignant ovarian tumours

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