Apoptosis in endometrial glandular and stromal cells in women with and without endometriosis

Dmowski, W. Paul; Ding, Jane; Shen, Jikun; Rana, Nasir; Fernandez, Balbino B.; Braun, DP

doi:10.1093/humrep/16.9.1802

Cited by 210 publications

(134 citation statements)

References 32 publications

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“…In addition, compelling molecular evidence has shown fundamental differences in the endometrium from women with endometriosis compared to endometrium from women without endometriosis. Endometrium from women with endometriosis seems to have decreased expression of integrin [16] and HOXA10 [17], alterations in apoptosis [18], and a gene expression profile consistent with progesterone resistance [19]. We did not evaluate molecular data in this study and the only measure of endometrial receptivity we studied, endometrial thickness, was similar in patients before and after surgery ( Table 2).…”

Section: Discussionmentioning

confidence: 95%

Embryo quality before and after surgical treatment of endometriosis in infertile patients

Shahine

Burney

Behr

et al. 2009

J Assist Reprod Genet

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Section: Discussionmentioning

confidence: 95%

Embryo quality before and after surgical treatment of endometriosis in infertile patients

Shahine

Burney

Behr

et al. 2009

J Assist Reprod Genet

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“…Apoptotic cells were detected with an ELISA-based cell death detection kit (14) or the TUNEL assay for DNA fragmentation (15). To evaluate cell death repressor activity, bcl-2 was also determined by immunohistochemistry (16)(17)(18)(19)(20).…”

Section: Discussionmentioning

confidence: 99%

Reduction of apoptosis and proliferation in endometriosis

Béliard

Noël

Foidart

2004

Fertility and Sterility

151

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Objective: To evaluate whether endometriosis could be related to an impaired balance between apoptosis and proliferation, two processes which could be modulated by hormonal status.Design: Immunohistochemical study.Setting: Academic research laboratory. Intervention(s):Endometriotic samples obtained from peritoneum of women aged 26-40 years who were undergoing laparoscopy for pain or infertility. Main Outcome Measure(s):Apoptotic cells were detected with the use of the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay. The production of p53 and bcl-2, estrogen and Progesterone (P) receptors, and cellular proliferation were assessed by immunohistochemistry in eutopic and ectopic endometria from 30 patients with endometriosis throughout the menstrual cycle. Results were compared with those from normal endometria from 15 fertile patients. Result(s):Endometriotic lesions were characterized by reduced TUNEL and p53 stainings and by enhanced bcl-2 staining. No correlation between apoptosis and estrogen receptor or P receptor levels was found. A lower amount of steroid receptor was found in endometriotic tissues, without cyclic modulation, compared with the eutopic endometrium. Conclusion(s):Our results suggest that when endometrial tissue is located at ectopic locations, it differs from eutopic endometrium by its proliferation rate, steroid hormone levels, and markers of apoptosis. A reduced sensitivity of endometriotic cells to apoptosis could promote the dissemination and implantation of these cells to ectopic sites.

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“…Accumulated evidence indicates that decreased apoptosis of endometrial cells in a phase-dependent manner during the menstrual cycle may facilitate ectopic survival of implanted endometrial fragments (Dmowski et al 2001, Garcia-Velasco & Arici 2003. In healthy women, the endometrium that is refluxed into the peritoneum undergoes apoptosis called anoikis because of its failure to interact with the extracellular matrix required for the growth of ectopic endometrium (Béliard et al 2004).…”

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

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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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Apoptosis in endometrial glandular and stromal cells in women with and without endometriosis

Cited by 210 publications

References 32 publications

Embryo quality before and after surgical treatment of endometriosis in infertile patients

Embryo quality before and after surgical treatment of endometriosis in infertile patients

Reduction of apoptosis and proliferation in endometriosis

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

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