ArticleInflammation2014
IL-1β Upregulates IL-8 Production in Human Müller Cells Through Activation of the p38 MAPK and ERK1/2 Signaling Pathways.
Article in Inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 69 citations in OpenAlex.
- NLRP3 inflammasome activation by particles and fibers: implications for human hazard assessment.Archives of toxicology · 2026Review
- Molecular stress and neurovascular injury in the diabetic retina.The Journal of clinical investigation · 2026Review
- Focusing on inflammation-driven pyroptosis in postherpetic neuralgia: from molecular mechanisms to therapeutic strategies.Frontiers in immunology · 2026Review
- The diabetic retina-brain axis hypothesis in diabetic cognitive impairment: from pathophysiological mechanisms to therapeutic implications.Frontiers in endocrinology · 2026Review
- Retinal ALKBH5 inhibition induces myopia protection through selective regulation of ERK1/2 signaling.Journal of translational medicine · 2025Article
- Jamamina: A Green Nanostructured Lipid Carrier with NaDES and Curcumin for Redox Modulation and Inflammatory Disorders.International journal of molecular sciences · 2025Article
- The role of intestinal macrophage polarization in colitis-associated colon cancer.Frontiers in immunology · 2025Review
- MAPK/ERK signaling pathway in rheumatoid arthritis: mechanisms and therapeutic potential.PeerJ · 2025Review
- Acute COVID-19 and LongCOVID syndrome - molecular implications for therapeutic strategies - review.Frontiers in immunology · 2025Review
- Understanding chronic inflammation: couplings between cytokines, ROS, NO, CaFrontiers in immunology · 2025Review
- Induction, amplification, and propagation of diabetic retinopathy-associated inflammatory cytokines between human retinal microvascular endothelial and Müller cells and in the mouse retina.Cellular signalling · 2024Article
- Glutathione trisulfide prevents lipopolysaccharide-induced retinal inflammation via inhibition of proinflammatory cytokine production in glial cells.Scientific reports · 2023Article
- Phosphorylation of αB-Crystallin Involves Interleukin-1β-Mediated Intracellular Retention in Retinal Müller Cells: A New Mechanism Underlying Fibrovascular Membrane Formation.Investigative ophthalmology & visual science · 2023Article
- Inhibition of Galectins and the P2X7 Purinergic Receptor as a Therapeutic Approach in the Neurovascular Inflammation of Diabetic Retinopathy.International journal of molecular sciences · 2023Review
- Article
- The ideal treatment timing for diabetic retinopathy: the molecular pathological mechanisms underlying early-stage diabetic retinopathy are a matter of concern.Frontiers in endocrinology · 2023Review
- Effect of cytokine-induced alterations in extracellular matrix composition on diabetic retinopathy-relevant endothelial cell behaviors.Scientific reports · 2022Article
- Single-cell transcriptomic analysis revealing changes in retinal cell subpopulation levels and the pathways involved in diabetic retinopathy.Annals of translational medicine · 2022Article
- Inhibiting the activation of MAPK (ERK1/2) in stressed Müller cells prevents photoreceptor degeneration.Theranostics · 2022Article
- Rapamycin and Resveratrol Modulate the Gliotic and Pro-Angiogenic Response in Müller Glial Cells Under Hypoxia.Frontiers in cell and developmental biology · 2022Article
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 3 countries.
Funding
Abstract
Diabetic retinopathy shares some similarity with chronic inflammation and Müller cells dysfunction may play an important role in its initiation and progression since these cells are thought to be a major source of inflammatory factors. The goal of this study was to examine the effect of cytokines on human retinal Müller cells and to understand the underlying signal transduction pathways regulating interleukin-8 (IL-8) expression. In this study, human MIO-M1 cells were treated with interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), IL-8, vascular endothelial growth factor (VEGF), interferon-gamma (IFN-γ), glucose, or mannitol, followed by examination of their IL-8 protein and mRNA levels by Western blotting and PCR, respectively. After treatment with IL-1β, the levels of phosphorylated p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated protein kinases 1 and 2 (ERK1/2), c-Jun N-terminal kinase (JNK), Janus kinase 2 (JAK2), and signal transducer and activator of transcription 3 (STAT3) were measured. IL-8 was also measured by Western blotting and ELISA following Müller cell culture with IL-1β and specific inhibitors of the p38 MAPK, ERK1/2, JNK, or JAK2 pathways. The results showed that IL-1β was a potent inducer of IL-8 expression in MIO-M1 cells, although a relatively small increase was induced by TNF-α. IL-6, IL-8, VEGF, and IFN-γ did not modify IL-8 expression. Increase of IL-8 expression was accompanied by a significant increased phosphorylation of p38 MAPK, ERK, and JNK, but not of JAK2 and STAT3. Furthermore, inhibitors of p38 MAPK and MEK1/2, but not for JNK and JAK2, significantly inhibited IL-8 expression. In conclusion, IL-1β potently stimulates IL-8 expression in Müller cells mainly through the p38 MAPK and ERK1/2 pathways.
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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.