Higher Follicular Fluid Progesterone Down-regulated HPGD and COX2 in Granulosa Cells via Suppressing NF-кB Signaling in Endometriosis

Jingyi Li, Jianpeng Chen, Yuli Qian, Junyan Ma, Fei-Da Ni, Yifeng Lin, Runju Zhang, Siwen Wang, Yun Huang, Juan Liu, Mixue Tu, Yanyun Ying, Yiqing Wu, Xuechen Wu, WU Bing-bing, Bo Zhu, Dan Zhang
In: Research Square · 2021 · doi:10.21203/rs.3.rs-882586/v1 · W3200878029
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⚙ AI-generated summary by claude@2026-06+body, 2026-06-10 ⓘ

Elevated follicular fluid progesterone in endometriosis patients suppresses NF-κB signaling, down-regulating HPGD and COX2 expression in granulosa cells.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-10 ⓘ

This preprint investigated how elevated progesterone in follicular/peritoneal fluid affects granulosa cells and ovulation-associated pathways in patients with endometriosis, using matched pairs from 50 ovarian endometriosis patients and 50 controls undergoing IVF/ICSI plus in vitro experiments in KGN granulosa tumor-like cells. It found that endometriosis patients had higher progesterone levels in serum and in follicular/peritoneal fluid, along with reduced granulosa cell expression of HPGD and COX-2 and suppressed NF-κB signaling (including decreased IL1R1 and IRAK3), while in vitro progesterone dose-dependently down-regulated HPGD and COX-2 and reduced NF-κB activity markers (lower pIκBα/IκBα ratio and reduced p65 nuclear translocation), with ChIP identifying a potential p65 binding site in the HPGD promoter; TNF-α showed opposite effects. A key limitation is that mechanistic conclusions rely heavily on a cell line model (KGN) rather than primary granulosa cells, and the study is presented as an unreviewed preprint. This paper is centrally about endometriosis—specifically, it links endometriosis-associated elevated follicular progesterone to down-regulation of HPGD and COX-2 via suppressed NF-κB signaling in granulosa cells and its proposed connection to LUFS/infertility.

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endometriosis

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