ArticleInternational journal of clinical and experimental pathology2013
Indoleamine 2,3-dioxygenase-1 (IDO1) enhances survival and invasiveness of endometrial stromal cells via the activation of JNK signaling pathway.
Article in International journal of clinical and experimental pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Endometrial biomarkers for the non-invasive diagnosis of endometriosis.The Cochrane database of systematic reviews · 2016Pooled it
- Pilot Study of the Tart Cherry Juice for the Treatment of Insomnia and Investigation of Mechanisms.American journal of therapeuticsTrial
- The interaction between inflammation and estrogen in adenomyosis : from molecular mechanisms to therapeutic strategies.Seminars in immunopathology · 2026Review
- Endometriosis - on the intersection of modern environmental pollutants and ancient genetic regulatory variants.European journal of human genetics : EJHG · 2026Article
- Leveraging epigenetic aberrations in the pathogenesis of endometriosis: from DNA methylation to non-coding RNAs.Frontiers in genetics · 2025Review
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- Higher Oxidative Stress in Endometriotic Lesions Upregulates Senescence-Associated p16International journal of molecular sciences · 2023Article
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- Article
- ARG1 mRNA Level Is a Promising Prognostic Marker in Head and Neck Squamous Cell Carcinomas.Diagnostics (Basel, Switzerland) · 2021Article
- Endometriosis Cell Proliferation Induced by Bone Marrow Mesenchymal Stem Cells.Reproductive sciences (Thousand Oaks, Calif.) · 2021Article
- IFN-γ and CD38 in Hyperprogressive Cancer Development.Cancers · 2021Review
- The Effect of Mesenchymal Stromal Cells Derived From Endometriotic Lesions on Natural Killer Cell Function.Frontiers in cell and developmental biology · 2021Article
- IDO1 depletion induces an anti-inflammatory response in macrophages in mice with chronic viral myocarditis.Cell cycle (Georgetown, Tex.) · 2019Article
- Anti-inflammatory cytokines in endometriosis.Cellular and molecular life sciences : CMLS · 2019Review
- Cyclooxygenase-2 in Endometriosis.International journal of biological sciences · 2019Review
- HAmerican journal of translational research · 2018Article
- Article
- IgA/IgM responses to tryptophan and tryptophan catabolites (TRYCATs) are differently associated with prenatal depression, physio-somatic symptoms at the end of term and premenstrual syndrome.Molecular neurobiology · 2017Article
- Mesenchymal Stromal Cells Are More ImmunosuppressiveStem cells international · 2017Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Evidence for an immunosuppressive function of indoleamine 2,3-dioxygenase (IDO) has been accumulating. However, the unusual distribution of IDO1 in gynecologic cancer cells suggests that modulating immunity may not its only function. To clarify the physiological importance of IDO1 in endometriosis, a tumor-like benign disease, we have investigated the potential mechanism by which IDO1 modulated endometrial stromal cells (ESCs) proliferation and invasion. ESCs were obtained from 16 control women (normal) and 14 patients with ovarian endometrioma, then the normal ESCs were treated with plasmid pEGFP-N1-IDO1 or SD11-IDO1 short hairpin RNA (shRNA) alone, or in combination with c-Jun N-terminal kinase (JNK) inhibitor (SP600125), and subjected to cell viability, proliferation, apoptosis assay and Matrigel invasion assay. IDO1 mRNA expression was evaluated by quantitative real-time reverse transcription-polymerase chain reaction (real-time PCR), and protein levels of IDO1, survivin, protein 53 (p53), matrix metalloproteinase (MMP)-2, MMP-9, tissue-inhibitor of metalloproteinase-1 (TIMP-1) and cyclooxygenase-2 (COX-2) in IDO1-overexpressing and IDO1-deficiency ESCs were analyzed by in-cell Western. We found that IDO1 expression was higher in endometriosis-derived eutopic and ectopic ESCs, compared with endometriosis-free normal ESCs. As a result, IDO1-overexpression in ESCs was markedly linked to reduction of apoptosis and p53 expression, and upregulation of survival, proliferation, invasion, as well as expression of MMP-9, COX-2 expression, rather than expression of survivin, MMP-2 and TIMP-1. Reversely, JNK blockage could abrogate these alterations of ESCs in IDO1-overexpressing milieu, suggesting that JNK signaling pathway was indispensable for ESCs survival, proliferation and invasion enhanced by IDO1, which may contribute to the pathophysiology of endometriosis.
Indexed as
Identifiers
23411497PMC3563200W156853574What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.