ArticleImmune network2010
NDRG2-mediated Modulation of SOCS3 and STAT3 Activity Inhibits IL-10 Production.
Article in Immune network, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 28 citations in OpenAlex.
- A Novel Role of Neutrophil Elastase in Podocyte Dysfunction Induced by High Glucose, PMA, and MDP.Journal of cellular physiology · 2025Article
- Dual roles of innate immune cells and cytokines in shaping the breast cancer microenvironment.Frontiers in immunology · 2025Review
- The Function of N-Myc Downstream-Regulated Gene 2 (NDRG2) as a Negative Regulator in Tumor Cell Metastasis.International journal of molecular sciences · 2022Review
- NDRG2 Expression in Breast Cancer Cells Downregulates PD-L1 Expression and Restores T Cell Proliferation in Tumor-Coculture.Cancers · 2021Article
- The Inflammatory Cytokine Profile of Patients with Malignant Pleural Effusion Treated with Pleurodesis.Journal of clinical medicine · 2020Article
- Astrocyte-specific NDRG2 gene: functions in the brain and neurological diseases.Cellular and molecular life sciences : CMLS · 2020Review
- Prolonged Release and Functionality of Interleukin-10 Encapsulated within PLA-PEG Nanoparticles.Nanomaterials (Basel, Switzerland) · 2019Article
- Engulfment, persistence and fate of Bdellovibrio bacteriovorus predators inside human phagocytic cells informs their future therapeutic potential.Scientific reports · 2019Article
- [Research progress on nonspecific immune microenvironment in breast cancer].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2018Review
- Loss of NDRG2 in liver microenvironment inhibits cancer liver metastasis by regulating tumor associate macrophages polarization.Cell death & disease · 2018Article
- Neuropeptide FF increases M2 activation and self-renewal of adipose tissue macrophages.The Journal of clinical investigation · 2017Article
- Conditional independence mapping of DIGE data reveals PDIA3 protein species as key nodes associated with muscle aerobic capacity.Journal of proteomics · 2014Article
- Article
- Review
- NDRG2 Promotes GATA-1 Expression through Regulation of the JAK2/STAT Pathway in PMA-stimulated U937 Cells.Immune network · 2011Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundN-myc downstream regulated gene 2 (NDRG2) is a member of the NDRG gene family. Our previous report indicated a possible role for NDRG2 in regulating the cytokine, interleukin-10 (IL-10), which is an important immunosuppressive cytokine. Several pathways, including p38-MAPK, NF-κB, and JAK/STAT, are used for IL-10 production, and the JAK/STAT pathway can be inhibited in a negative feedback loop by the inducible protein, SOCS3. In the present study, we investigated the effect of NDRG2 gene expression on IL-10 signaling pathway that is modulated via SOCS3 and STAT3.
methodsWe generated NDRG2-overexpressing U937 cell line (U937-NDRG2) and treated the cells with PMA to investigate the role of NDRG2 in IL-10 production. U937 cells were also transfected with SOCS3- or NDRG2-specific siRNAs to examine whether the knockdown of SOCS3 or NDRG2 influenced IL-10 expression. Lastly, STAT3 and SOCS3 induction was measured to identify the signaling pathway that was associated with IL-10 production.
resultsRT-PCR and ELISA assays showed that IL-10 was increased in U937-mock cells upon stimulation with PMA, but IL-10 was inhibited by overexpression NDRG2. After PMA treatment, STAT3 phosphorylation was decreased in a time-dependent manner in U937-mock cells, whereas it was maintained in U937-NDRG2 cells. SOCS3 was markedly reduced in U937-NDRG2 cells compared with U937-mock cells. IL-10 production after PMA stimulation was reduced in U937 cells when SOCS3 was inhibited, but this effect was less severe when NDRG2 was inhibited.
conclusionNDRG2 expression modulates SOCS3 and STAT3 activity, eventually leading to the inhibition of IL-10 production.
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