Protein arginine methyltransferase 5 mediates THP‑1‑derived macrophage activation dependent on NF‑κB in endometriosis
- Xiaoshan Chai
- Xianqing Wu
- Ling He
- Hui Ding
Affiliations: Department of Obstetrics and Gynecology, The Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, P.R. China
- Published online on: July 15, 2021 https://doi.org/10.3892/etm.2021.10436
Copyright: © Chai
et al. This is an open access article distributed under the
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Macrophage‑induced inflammation is a major factor in the pathogenesis of endometriosis. The underlying mechanisms, however, remain largely unknown. TNF‑α, IL‑6, IL‑10 and C‑C motif chemokine 20 (CCL20) levels in endometrial extracts were determined using Luminex cytokine kits. Additionally, protein arginine methyltransferase 5 (PRMT5) levels were measured using reverse transcription‑quantitative PCR and western blotting. IL‑6 and IP‑10 levels in cells were measured using ELISA kits. In the present study, it was revealed that PRMT5 expression at both the mRNA and protein levels in THP‑1‑derived macrophages was significantly decreased following treatment with serum or extracts of endometrium from patients with endometriosis in the presence of lipopolysaccharide, compared with that in control cells, suggesting a possible role for macrophage‑derived PRMT5 in mediating the interaction between macrophages and endometrium in endometriosis. Mechanistically, macrophage PRMT5 expression was regulated in an NF‑κB‑dependent and Smad2/3‑independent manner, indicating that PRMT5 is a downstream target of NF‑κB. Importantly, macrophage‑derived PRMT5 was required for macrophage activation in endometriosis, as evidenced by the PRMT5‑dependent secretion of IL‑6 and IFN‑γ‑induced protein 10 from THP‑1‑derived macrophages. The present study identified NF‑κB‑dependent PRMT5 as a novel regulator of macrophage activation in endometriosis. Targeting PRMT5 in macrophages may be a potential therapeutic strategy against endometriosis.