ArticleAnnals of translational medicine2021
Tumor necrosis factor receptor type 1-associated death domain (TRADD) regulates epithelial-mesenchymal transition (EMT), M1/M2 macrophage polarization and ectopic endometrial cysts formation in endometriosis.
Article in Annals of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 12 citations in OpenAlex.
- The inhibition of deep peritoneal endometriosis by Andrographolide through macrophage M1 activity in an endometriosis mice model.Veterinarni medicina · 2026Article
- Changes in the M1/M2 ratio due to andrographolide therapy for deep endometriosis: An experimental study using a BALB/C endometriosis model.Open veterinary journal · 2025Article
- TRADD-mediated pyroptosis contributes to diabetic cardiomyopathy.Acta pharmacologica Sinica · 2025Article
- Oral Cancer Stem Cell-Derived Small Extracellular Vesicles Promote M2 Macrophage Polarization and Suppress CD4Stem cells international · 2022Article
- Understanding the molecular mechanisms of macrophage polarization and metabolic reprogramming in endometriosis: A narrative review.Reproductive medicine and biologyReview
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Authors and funding
5 authors at 2 institutions in 1 country.
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Abstract
backgroundEndometriosis is a gynecological non-malignant disease that is manifested by the presence of extrauterine ectopic endometrial cells and stroma. The aim of current study was to explore the role of tumor necrosis factor receptor type 1-associated death domain (TRADD) protein in endometriosis.
methodsCell migration, invasion, and the expression of epithelial-mesenchymal transition (EMT) inducers in TRADD silencing or overexpression in eutopic endometrial stromal cells (EuSCs) and ectopic endometrial stromal cells (EcSCs) were analyzed by wound healing assay, transwell assay, quantitative reverse transcription polymerase chain reaction (qRT-PCR), western blotting and rat endometriosis model. A cell line derived from THP-1 macrophages was used to measure M1/M2 polarization in endometriosis by flow cytometry and enzyme-linked immunosorbent assay (ELISA).
resultsThe mRNA level and protein expression of TRADD, keratin, E-cadherin, N-cadherin, vascular endothelial growth factor, matrix metalloproteinase-9, CD40, and CD206 were abnormally expressed in ectopic endometrial tissues and EcSCs. TRADD silencing promoted migration, invasion, and EMT in EuSCs, while TRADD overexpression restrained migration, invasion, and EMT in EcSCs. TRADD knockdown prohibited M1/M2 polarization in normal endometrial homogenization-treated THP-1-derived macrophages, whereas TRADD upregulation facilitated M1/M2 polarization in patients with endometrial homogenization-treated THP-1-derived macrophages. In addition, TRADD overexpression suppressed ectopic endometrial cysts formation in a rat endometriosis model. TRADD overexpression activated NF-κB and MAPK signaling in EcSCs and rat models.
conclusionsOur results indicated that the overexpression of TRADD prohibited migration, invasion, EMT, M1/M2 polarization and ectopic endometrial cysts formation in endometriosis, and this might due to regulating NF-κB and MAPK signaling.
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