Elevated soluble Fas ligand levels may suggest a role for apoptosis in women with endometriosis

García-Velasco, Juan A.; Mulayim, Naciye; Kayisli, Umit A.; Arıcı, Aydın

doi:10.1016/s0015-0282(02)03320-4

Cited by 68 publications

(39 citation statements)

References 29 publications

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“…Our findings suggest that low levels of sFas may be associated with increase of apoptotic activity in IVF patients with different causes of infertility. In a study about serum sFasL levels in women with endometriosis, elevated sFasL levels were found in patients compare with fertile women without endometriosis [22]. They think that women with endometriosis is susceptible to apoptosis more thanwomen without disease.…”

Section: Discussionmentioning

confidence: 97%

Changes of sFas and sFasL, oxidative stress markers in serum and follicular fluid of patients undergoing IVF

Pekel

Gönenç

Turhan

et al. 2014

J Assist Reprod Genet

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Purpose The Fas-Fas Ligand interaction is one of the essential events for the induction of apoptosis whereas the exact role of their soluble forms in the reproductive system is still not fully understood. Also oxidative stress in the pathogenesis of infertility causing diseases in women and has been suggested as one of the important factors that negatively affect IVF outcome. In this study, our aim was to evaluate serum and follicular fluid levels of soluble Fas soluble Fas Ligand, malondialdehyde, superoxide dismutase and total antioxidant capacity in patients undergoing IVF and compared with controls. Methods This study included 109 patients. Patients were classified as unexplained infertility (N=31), PCOS (N=19), tubal factor (N=9) and endometriosis (N=10) and compared with male factor infertility (N=40) that was the control group. sFas and sFasL levels were measured by immunoassay method. MDA, SOD and TAC levels were measured by colorimetric method. Results Patients with unexplained infertility, PCOS and tubal factor had significantly lower sFas levels compared with their controls (respectively, p<0.01, p<0.05, p<0.05). However, SOD activity in unexplained infertility, PCOS and endometriosisgroupswere significantly higher than control group (p<0.01).Decreased follicular fluid TAC levels were found in all patient groups compared with controls (respectively, p<0.01, p<0.05, p<0.01, p<0.01).Patients with tubal factor had significantly higher serum sFasL (p<0.05), but lower follicular fluid sFasL levels (p<0.05) compared with unexplained infertility. Tubal factor and endometriosis groups had lowerfollicular fluid TAC levels compared to unexplained infertility and PCOSgroups (p<0.01). Conclusion(s) In this study, serum and follicular fluid sFas levels were decreased and antioxidant activity was impaired in infertility, possibly implying increased apoptosis. Especially in unexplained infertility group changes in this parametres more remarkable.

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Section: Discussionmentioning

confidence: 97%

Changes of sFas and sFasL, oxidative stress markers in serum and follicular fluid of patients undergoing IVF

Pekel

Gönenç

Turhan

et al. 2014

J Assist Reprod Genet

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“…Substantial evidence links NFKB to antiapoptotic and proapoptotic effects, through the BCL2 family and the FAS/FASLG complex (Lee et al 1999, Pahl 1999, Wang et al 1999, Harada et al 2004. In ectopic and/or eutopic endometria from endometriosis patients, endometrial cell viability is mainly controlled by the overexpression of BCL2 and a decreased expression of BAX and FAS molecules (Meresman et al 2000, Garcia-Velasco et al 2002, Johnson et al 2005, effects that may allow cell survival in ectopic sites. Although the reduced function of the NFKB system observed in our results does not explain the mechanism by which apoptosis is reduced in eutopic endometrium from endometriosis patients, in other pathologies such as adenomyosis, defined as the presence of ectopic endometrium within the myometrium, the decrease in apoptosis was regulated by mediators other than BCL2 (Yang et al 2007), while in breast cancer and in B-cell leukaemia an association between enhanced expression of BCL2 and NFKB2, other NFKB heterodimers, was shown (Viatour et al 2003).…”

Section: Discussionmentioning

confidence: 99%

Nuclear factor κB pathway and interleukin-6 are affected in eutopic endometrium of women with endometriosis

Ponce¹,

Torres²,

Galleguillos³

et al. 2009

Reproduction

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In order to investigate the role of the nuclear factor kB (NFKB) pathway on gene expression in the eutopic endometrium in endometriosis, and in particular of interleukin-6 (IL6), we evaluated RELA, IkB kinase (CHUK), NFKBIA and IL6 expressions and NFKB DNA binding in eutopic endometrium from women with endometriosis. Eutopic endometrium was obtained from 37 women with endometriosis and 42 fertile women during laparoscopy. We analysed RELA, CHUK, NFKBIA and IL6 mRNA levels (RT-PCR); RELA, CHUK and NFKBIA proteins and p-NFKBIA/NFKBIA ratio (western blot); and NFKB binding (DNA shift assay) and IL6 concentration (ELISA) in endometrial explants. Our results indicate that mRNA and cytoplasmic proteins of RELA and CHUK exhibit constant levels in normal endometrium during the menstrual cycle. A dramatic increase (P!0.05) in NFKBIA mRNA expression, RELA nuclear presence and the mRNA and the protein of IL6 during late secretory phase was also observed in this tissue. By contrast, in eutopic endometrium from endometriosis patients, a decrease (P!0.05) in IL6 mRNA and protein (61%), NFKBIA mRNA (46%), p-NFKBIA/NFKBIA ratio (42%), RELA nuclear stromal (68%) and CHUK (48%) proteins were found exclusively during the late secretory phase compared with normal endometrium. In conclusion, the canonical activation of NFKB pathway is deregulated and may have reduced transcriptional function affecting NFKBIA and IL6 expression, genes related local proinflammatory processes. These molecular alterations observed during the late secretory phase in eutopic endometrium from endometriosis patients constitute a NFKB system dysfunction, suggesting that NFKB could be an important factor in endometriosis aetiology.

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“…Apoptosis of eutopic and ectopic endometrial tissues may be less relied on FAS expression (Agic et al 2009). A study by Garcia-Velasco et al (2002) showed that elevated apoptosis of FAS-expressing immune cells in the peritoneal cavity of women with advanced endometriosis is attributed to high levels of soluble FASLG, impairing the removal of ectopic endometrial cells. This suggests a role for apoptotic deregulation in the pathophysiology of endometriosis.…”

Section: R202 L Pirdel and M Pirdelmentioning

confidence: 99%

Role of iron overload-induced macrophage apoptosis in the pathogenesis of peritoneal endometriosis

Pirdel¹,

Pirdel²

2014

Reproduction

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This article presents an overview of the involvement of iron overload-induced nitric oxide (NO) overproduction in apoptosis of peritoneal macrophages of women with endometriosis. We have postulated that the peritoneal iron overload originated from retrograde menstruation or bleeding lesions in the ectopic endometrium, which may contribute to the development of endometriosis by a wide range of mechanisms, including oxidative damage and chronic inflammation. Excessive NO production may also be associated with impaired clearance of endometrial cells by macrophages, which promotes cell growth in the peritoneal cavity. Therefore, further research of the mechanisms and consequences of macrophage apoptosis in endometriosis helps discover novel therapeutic strategies that are designed to prevent progression of endometriosis.

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Elevated soluble Fas ligand levels may suggest a role for apoptosis in women with endometriosis

Cited by 68 publications

References 29 publications

Changes of sFas and sFasL, oxidative stress markers in serum and follicular fluid of patients undergoing IVF

Changes of sFas and sFasL, oxidative stress markers in serum and follicular fluid of patients undergoing IVF

Nuclear factor κB pathway and interleukin-6 are affected in eutopic endometrium of women with endometriosis

Role of iron overload-induced macrophage apoptosis in the pathogenesis of peritoneal endometriosis

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