Investigating the impact of local inflammation on granulosa cells and follicular development in women with ovarian endometriosis

Ying Li, Li Y, Ruiqi Li, Li R, Ouyang N, Nengyong Ouyang, Dai K, Kailing Dai, Ping Yuan, Lingyan Zheng, Zheng L, Wang W, Wenjun Wang
Fertility and sterility · 2019 · vol. 112(5) , pp. 882–891.e1 · doi:10.1016/j.fertnstert.2019.07.007 · PMID:31551156 · W2974547785
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This study investigated the effects of local inflammation associated with ovarian endometriosis on granulosa cells and the development of ovarian follicles in women.

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Abstract

ObjectiveTo investigate the possible impact of local inflammation on granulosa cells (GCs) and follicular development in endometriosis patients.DesignProspective study with related paired design.SettingReproductive medicine center.Patient(s)A total of 80 endometriosis patients and 104 controls, with cultured GCs collected from control participants younger than 35 years.Intervention(s)Tumor necrosis factor-α (TNF-α) and nuclear factor κB (NF-κB) inhibitor.Main outcome measure(s)Intrafollicular concentrations of cytokines measured with ELISA, NF-κB binding levels with electrophoretic mobility shift assay (EMSA), and telomerase activity (TA) with quantitative-telomeric repeat amplification protocol (Q-TRAP) assay, and protein and mRNA expression with Western blot and polymerase chain reaction analyses, respectively.Result(s)Patients with endometriosis exhibited a statistically significantly lower antral follicle count (11.48 ± 8.11 vs. 15.68 ± 8.56), lower number of retrieved oocytes (8.28 ± 6.69 vs. 10.87 ± 6.26), and lower number of mature oocytes (6.67 ± 6.09 vs. 8.53 ± 5.69). The GCs from endometriosis patients showed higher NF-κB binding activity and increased expression of inhibitor of NF-κB kinase subunit β (IKKβ, 2.743-fold) and NF-κB inhibitor α (IκBα, 5.017-fold). Their NF-κB p65 expression was negatively associated with mature oocytes (bNF-κB' = -0.304, R2 = 0.195, R = 0.442) but positively associated with intrafollicular TNF-α (r = 0.37); TA showed a negative relationship with NF-κB binding levels (r = -0.667). Tumor necrosis factor-α induced expression of IκBα (5.408-fold) and NF-κB p65 (1.400-fold) but lowered human telomerase reverse transcriptase (hTERT) and TA levels (0.0009 vs. 0.5619) in cultured GCs. However, inhibiting NF-κB obviously increased hTERT expression (1.988-fold).Conclusion(s)Endometriosis showed activated NF-κB pathways in GCs, which might negatively affect TA and oocyte quality. Intrafollicular TNF-α might down-regulate TA and hTERT via NF-κB pathway, but further studies are required.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometriosis Granulosa Cells Inflammation Mediators Ovarian Follicle Ovarian Follicle Adult Cells, Cultured Endometriosis Female Granulosa Cells Humans Inflammation Inflammation Inflammation Inflammation Mediators NF-kappa B NF-kappa B Ovarian Follicle Pregnancy

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