ArticleOncotarget2015
Oncoprotein mdig contributes to silica-induced pulmonary fibrosis by altering balance between Th17 and Treg T cells.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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
31 citing papers in PubMed.
- The Paeonol of Total Glucosides of White Peony Regulates the Differentiation of CD4+Treg Cells through the EP300/Foxp3 Axis to Relieve Pulmonary Fibrosis in Mice.Cell biochemistry and biophysics · 2025Article
- Epigenetic regulation of breast cancer metastasis.Cancer metastasis reviews · 2024Review
- Predicting role of Myc-induced nuclear antigen 53 in determining the development and severity of systemic lupus erythematosus.Frontiers in immunology · 2024Article
- Deletion of mdig enhances H3K36me3 and metastatic potential of the triple negative breast cancer cells.iScience · 2022Article
- JMJD family proteins in cancer and inflammation.Signal transduction and targeted therapy · 2022Review
- Depletion ofBiomedicines · 2022Article
- MDIG, a 2‑oxoglutarate‑dependent oxygenase, acts as an oncogene and predicts the prognosis of multiple types of cancer.International journal of oncology · 2022Article
- Epigenetics and environment in breast cancer: New paradigms for anti-cancer therapies.Frontiers in oncology · 2022Review
- Cooperation between NRF2-mediated transcription and MDIG-dependent epigenetic modifications in arsenic-induced carcinogenesis and cancer stem cells.Seminars in cancer biology · 2021Review
- Pathological and Prognostic Indications of the mdig Gene in Human Lung Cancer.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2021Article
- Emergency myelopoiesis contributes to immune cell exhaustion and pulmonary vascular remodelling.British journal of pharmacology · 2021Article
- Environmentally-inducedTheranostics · 2021Article
- RNA-seq-Based Screening in Coal Dust-Treated Cells IdentifiedBioMed research international · 2021Article
- Interpreting Immunoregulation in Lung Fibrosis: A New Branch of the Immune Model.Frontiers in immunology · 2021Review
- CRISPR-Cas9 gene editing causes alternative splicing of the targeting mRNA.Biochemical and biophysical research communications · 2020Article
- Mdig promotes oncogenic gene expression through antagonizing repressive histone methylation markers.Theranostics · 2020Article
- MDIG promotes cisplatin resistance of lung adenocarcinoma by regulating ABC transporter expression via activation of the WNT/β-catenin signaling pathway.Oncology letters · 2019Article
- New discoveries of mdig in the epigenetic regulation of cancers.Seminars in cancer biology · 2019Review
- The emerging roles of ribosomal histidyl hydroxylases in cell biology, physiology and disease.Cellular and molecular life sciences : CMLS · 2018Review
- A SNP uncoupling Mina expression from the TGFβ signaling pathway.Immunity, inflammation and disease · 2018Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Mineral dust-induced gene (mdig, also named Mina53) was first identified from alveolar macrophages of the coal miners with chronic lung inflammation or fibrosis, but how this gene is involved in lung diseases is poorly understood. Here we show that heterozygotic knockout of mdig (mdig+/-) ameliorates silica-induced lung fibrosis by altering the balance between Th17 cells and Treg cells. Relative to the wild type (WT) mice, infiltration of the macrophages and Th17 cells was reduced in lungs from silica-exposed mdig+/- mice. In contrast, an increased infiltration of the T regulatory (Treg) cells to the lung intestitium was observed in the mdig+/- mice treated with silica. Both the number of Th17 cells in the lung lymph nodes and the level of IL-17 in the bronchoalveolar lavage fluids were decreased in the mdig+/- mice in response to silica. Thus, these results suggest that mdig may contribute to silica-induced lung fibrosis by altering the balance between Th17 and Treg cells. Genetic deficiency of mdig impairs Th17 cell infiltration and function, but favors infiltration of the Treg cells, the immune suppressive T cells that are able to limit the inflammatory responses by repressing the Th17 cells and macrophages.
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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.