Apoptosis and proliferative activity in endometrium during peritoneal endometriosis

Бурлев, В. А.; Павлович, С. В.; Ilyasova, N. A.

doi:10.1007/s10517-006-0128-x

Cited by 10 publications

(4 citation statements)

References 8 publications

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“…For instance, many changes have been found in both the ultrastructral morphology and the molecular composition of the endometrium in patients with endometriosis, providing the basis for a uterine factor in infertility (15)(16)(17). Likewise, polycystic ovary syndrome has also been characterized with specific alterations in the endometrium, including a change in the ratio of estrogen and androgen receptors (18,19).…”

Section: Introductionmentioning

confidence: 99%

Defining the proliferative phase endometrial defect

Bromer

Aldad

Taylor

2009

Fertility and Sterility

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Objective-To evaluate proliferative phase endometrial development in a heterogeneous infertility population.Design-Retrospective study. Patient(s)-246 treatment cycles.Setting-University-based infertility practice. Intervention(s)-Clomiphene citrate or FSH ovarian stimulation, followed by intrauterine insemination or in vitro fertilization.Main Outcome Measures(s)-Endometrial thickness by transvaginal ultrasonography. Clinical pregnancy rate.

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Section: Introductionmentioning

confidence: 99%

Defining the proliferative phase endometrial defect

Bromer

Aldad

Taylor

2009

Fertility and Sterility

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“…Nevertheless, in our study, the apoptosis rate of the ect-MSCs was not determined along with the inhibition of NOD1 expression. Liu et al (24) found that ect-MSCs exhibited a higher level of proliferation, while Burlev et al (25) observed no difference in the proliferation abilities between ect-MSCs and eut-MSCs. Overall, our study uncovered that the NOD1 li-gand Tri-DAP can promote the proliferation of eut-MSCs.…”

Section: Discussionmentioning

confidence: 99%

Human Endometrium Derived Mesenchymal Stem Cells with Aberrant NOD1 Expression Are Associated with Ectopic Endometrial Lesion Formation

Li,

Luo,

Guo

et al. 2024

Int J Stem Cells

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Nucleotide-binding oligomerization domain 1 (NOD1), a cytosolic pattern recognition receptor protein, plays a crucial role in innate immune responses. However, the functional expression of NOD1 in mesenchymal stem cells (MSCs) derived from endometriosis remains unclear. The aim of this study was to explore the functions of NOD1 in ectopic endometrial lesions. Tissues and MSCs were isolated from both normal endometrium and endometriosis. Immunohistochemistry and real time quantitative polymerase chain reaction (RT-qPCR) were used to determine the expression of NOD1 in the tissues/MSCs. Quantification of various cytokines was performed using RT-qPCR and enzyme-linked immunosorbent assay. To confirm the proliferation, invasion/migration, and apoptotic viabilities of the samples, Cell Counting Kit-8, clonogenic formation, transwell assays, and apoptotic experiments were conducted. Higher levels of NOD1 expression were detected in the ectopic-MSCs obtained from endometriosis compared to those from the endometrium. The expression of interleukin-8 was higher in the ectopic-MSCs than in the eutopic-MSCs. Pretreatment with NOD1 agonist significantly enhanced the proliferation and invasion/migration of eutopic-MSCs. Additionally, the NOD1 inhibitor ML-130 significantly reduced the proliferation, clone formation, invasion, and migration abilities of the ectopic-MSCs, having no effect on their apoptosis capacity. Our findings suggest that the expression of NOD1 in ectopic-MSCs may contribute to the progression of ectopic endometrial lesions.

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“…Many researchers have demonstrated that the eutopic endometrial cell is the essential factor for endometriosis development. 33,34 We used hESCs from patients with endometriosis to evaluate the effect of TNF-α and TNF-α inhibitors on the pathogenesis of endometriosis. Our results showed that TNF-α (0-10 ng/mL) stimulated hESC proliferation in a dose-responsive manner; 1 ng/mL TNF-α significantly promoted the hESC survival rate and S-phase percentage.…”

Section: Discussionmentioning

confidence: 99%

rhTNFR: Fc Suppresses the Development of Endometriosis in a Mouse Model by Downregulating Cell Proliferation and Invasiveness

et al. 2016

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Tumor necrosis factor α (TNF-α), a proinflammatory cytokine, may play an important role in the pathogenesis of endometriosis; therefore, TNF-α inhibitors potentially have an effect on endometriosis. To investigate the effect of anti-TNF-α treatment on endometriosis, 2 TNF-α inhibitors: recombinant human TNF receptor: Fc fusion protein (rhTNFR: Fc) and TNF-α monoclonal antibody (TNF-α mAb) were used to treat human eutopic endometrial stromal cells (hESCs), and the effects on cell survival, cell cycle, and invasiveness were compared. It was found that rhTNFR: Fc suppressed the TNF-α-induced hESC survival and invasiveness but not TNF-α mAb. Recombinant human TNF receptor: Fc fusion protein decreased the S phase of hESC compared with the TNF-α-treated group. Then, we used a surgically induced mouse model of endometriosis to study the effect of rhTNFR: Fc treatment in vivo. The fluorescence intensity and the size of implanted endometriotic lesions in the mouse model were decreased by rhTNFR: Fc. In conclusion, rhTNFR: Fc suppresses hESC survival and invasiveness and decreases the fluorescence intensity and implant size in the mouse model of endometriosis.

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Apoptosis and proliferative activity in endometrium during peritoneal endometriosis

Cited by 10 publications

References 8 publications

Defining the proliferative phase endometrial defect

Defining the proliferative phase endometrial defect

Human Endometrium Derived Mesenchymal Stem Cells with Aberrant NOD1 Expression Are Associated with Ectopic Endometrial Lesion Formation

rhTNFR: Fc Suppresses the Development of Endometriosis in a Mouse Model by Downregulating Cell Proliferation and Invasiveness

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