ArticleToxicological sciences : an official journal of the Society of Toxicology2016
Monomethylarsonous acid (MMA+3) Inhibits IL-7 Signaling in Mouse Pre-B Cells.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- Advances in IL-7 Research on Tumour Therapy.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Arsenite Methyltransferase Is an Important Mediator of Hematotoxicity Induced by Arsenic in Drinking Water.Water · 2023Article
- Chronic Community Exposure to Environmental Metal Mixtures Is Associated with Selected Cytokines in the Navajo Birth Cohort Study (NBCS).International journal of environmental research and public health · 2022Article
- Arsenite and monomethylarsonous acid disrupt erythropoiesis through combined effects on differentiation and survival pathways in early erythroid progenitors.Toxicology letters · 2021Article
- Arsenic methylation - Lessons from three decades of research.Toxicology · 2021Review
- Origins, fate, and actions of methylated trivalent metabolites of inorganic arsenic: progress and prospects.Archives of toxicology · 2021Review
- Gestational arsenic exposure induces site-specific DNA hypomethylation in active retrotransposon subfamilies in offspring sperm in mice.Epigenetics & chromatin · 2020Article
- Article
- Genotoxicity induced by monomethylarsonous acid (MMAToxicology letters · 2017Article
- Efflux Transporters Regulate Arsenite-Induced Genotoxicity in Double Negative and Double Positive T Cells.Toxicological sciences : an official journal of the Society of Toxicology · 2017Article
- Arsenic and Immune Response to Infection During Pregnancy and Early Life.Current environmental health reports · 2017Review
- Low level arsenite exposures suppress the development of bone marrow erythroid progenitors and result in anemia in adult male mice.Toxicology letters · 2017Article
- Differential sensitivities of bone marrow, spleen and thymus to genotoxicity induced by environmentally relevant concentrations of arsenite.Toxicology letters · 2016Article
- Environmentally relevant concentrations of arsenite and monomethylarsonous acid inhibit IL-7/STAT5 cytokine signaling pathways in mouse CD3+CD4-CD8- double negative thymus cells.Toxicology letters · 2016Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Our previously published data show that As(+3) in vivo and in vitro, at very low concentrations, inhibits lymphoid, but not myeloid stem cell development in mouse bone marrow. We also showed that the As(+3) metabolite, monomethylarsonous acid (MMA(+3)), was responsible for the observed pre-B cell toxicity caused by As(+3). Interleukin-7 (IL-7) is the primary growth factor responsible for pre-lymphoid development in mouse and human bone marrow, and Signal Transducer and Activator of Transcription 5 (STAT5) is a transcriptional factor in the IL-7 signaling pathway. We found that MMA(+3) inhibited STAT5 phosphorylation at a concentration as low as 50 nM in mouse bone marrow pre-B cells. Inhibition of STAT5 phosphorylation by As(+3) occurred only at a concentration of 500 nM. In the IL-7 dependent mouse pre-B 2E8 cell line, we also found selective inhibition of STAT5 phosphorylation by MMA(+3), and this inhibition was dependent on effects on JAK3 phosphorylation. IL-7 receptor expression on 2E8 cell surface was also suppressed by 50 nM MMA(+3) at 18 h. As further evidence for the inhibition of STAT5, we found that the induction of several genes required in B cell development, cyclin D1, E2A, EBF1, and PAX5, were selectively inhibited by MMA(+3). Since 2E8 cells lack the enzymes responsible for the conversion of As(+3) to MMA(+3) in vitro, the results of these studies suggest that As(+3) induced inhibition of pre-B cell formation in vivo is likely dependent on the formation of MMA(+3) which in turn inhibits IL-7 signaling at several steps in mouse pre-B cells.
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