ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Shaping the murine macrophage phenotype: IL-4 and cyclic AMP synergistically activate the arginase I promoter.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 67 citations in OpenAlex.
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- Selective phosphodiesterase 4 inhibitor roflumilast reduces inflammation and lung injury in models of betacoronavirus infection in mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Biochemistry, pharmacology, and in vivo function of arginases.Pharmacological reviews · 2025Review
- Mechanosensing regulates tissue repair program in macrophages.Science advances · 2024Article
- Advantages and disadvantages of treatment of experimental ARDS by M2-polarized RAW 264.7 macrophages.Heliyon · 2023Article
- Targeted ablation of signal transducer and activator of transduction 1 alleviates inflammation by microglia/macrophages and promotes long-term recovery after ischemic stroke.Journal of neuroinflammation · 2023Article
- Modulation of IL-4/IL-13 cytokine signaling in the context of allergic disease.The Journal of allergy and clinical immunology · 2022Review
- Taurodeoxycholic acid and valine reverse obesity-associated augmented alloimmune responses and prolong allograft survival.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2022Article
- Multifaceted Roles of cAMP Signaling in the Repair Process of Spinal Cord Injury and Related Combination Treatments.Frontiers in molecular neuroscience · 2022Review
- The Pivotal Immunoregulatory Functions of Microglia and Macrophages in Glioma Pathogenesis and Therapy.Journal of oncology · 2022Review
- Evidence for reprogramming of monocytes into reparative alveolar macrophages in vivo by targeting PDE4b.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Deficiency in ST2 signaling ameliorates RSV-associated pulmonary hypertension.American journal of physiology. Heart and circulatory physiology · 2021Article
- The Role of Macrophages in the Host's Defense againstPathogens (Basel, Switzerland) · 2021Review
- The Emerging Role of Macrophages in Immune System Dysfunction under Real and Simulated Microgravity Conditions.International journal of molecular sciences · 2021Review
- A data-driven computational model enables integrative and mechanistic characterization of dynamic macrophage polarization.iScience · 2021Article
- Treadmill Exercise Attenuates Cerebral Ischemia-Reperfusion Injury by Promoting Activation of M2 Microglia via Upregulation of Interleukin-4.Frontiers in cardiovascular medicine · 2021Article
- Transcriptional Profiling of Mouse Eosinophils Identifies Distinct Gene Signatures Following Cellular Activation.Frontiers in immunology · 2021Article
- Liquid PRF Reduces the Inflammatory Response and Osteoclastogenesis in Murine Macrophages.Frontiers in immunology · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Arginase I is a marker of murine M2 macrophages and is highly expressed in many inflammatory diseases. The basis for high arginase I expression in macrophages in vivo is incompletely understood but likely reflects integrated responses to combinations of stimuli. Our objective was to elucidate mechanisms involved in modulating arginase I induction by IL-4, the prototypical activator of M2 macrophages. IL-4 and 8-bromo-cAMP individually induce arginase I, but together they rapidly and synergistically induce arginase I mRNA, protein, and promoter activity in murine macrophage cells. Arginase I induction by IL-4 requires binding of the transcription factors STAT6 and C/EBPβ to the IL-4 response element of the arginase I gene. Chromatin immunoprecipitation showed that the synergistic response involves binding of both transcription factors to the IL-4 response element at levels significantly greater than in response to IL-4 alone. The results suggest that C/EBPβ is a limiting factor for the level of STAT6 bound to the IL-4 response element. The enhanced binding in the synergistic response was not due to increased expression of either STAT6 or C/EBPβ but was correlated primarily with increased nuclear abundance of C/EBPβ. Our findings also suggest that induction of arginase I expression is stochastic; that is, differences in induction reflect differences in probability of transcriptional activation and not simply differences in rate of transcription. Results of the present study also may be useful for understanding mechanisms underlying regulated expression of other genes in macrophages and other myeloid-derived cells in health and disease.
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