ArticlePLoS computational biology2016
Model-Based Characterization of Inflammatory Gene Expression Patterns of Activated Macrophages.
Article in PLoS computational biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 42 citations in OpenAlex.
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- Kisspeptin regulates airway hyperresponsiveness and remodeling in a mouse model of asthma.The Journal of pathology · 2023Article
- Systems biology of angiogenesis signaling: Computational models and omics.WIREs mechanisms of disease · 2022Review
- Anti-Inflammatory Effects of Cicadidae Periostracum Extract and Oleic Acid through Inhibiting Inflammatory Chemokines Using PCR Arrays in LPS-Induced Lung inflammation In Vitro.Life (Basel, Switzerland) · 2022Article
- IL-36α and Lipopolysaccharide Cooperatively Induce Autophagy by Triggering Pro-Autophagic Biased Signaling.Biomedicines · 2021Article
- Protocol for simulating macrophage signal transduction and phenotype polarization using a large-scale mechanistic computational model.STAR protocols · 2021Article
- RGS10 physically and functionally interacts with STIM2 and requires store-operated calcium entry to regulate pro-inflammatory gene expression in microglia.Cellular signalling · 2021Article
- A data-driven computational model enables integrative and mechanistic characterization of dynamic macrophage polarization.iScience · 2021Article
- Network Analysis Reveals a Distinct Axis of Macrophage Activation in Response to Conflicting Inflammatory Cues.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Transcriptional and Microenvironmental Landscape of Macrophage Transition in Cancer: A Boolean Analysis.Frontiers in immunology · 2021Article
- A generalizable data-driven multicellular model of pancreatic ductal adenocarcinoma.GigaScience · 2020Article
- Computational Approach to Identifying Universal Macrophage Biomarkers.Frontiers in physiology · 2020Article
- Deriving a Boolean dynamics to reveal macrophage activation with in vitro temporal cytokine expression profiles.BMC bioinformatics · 2019Article
- A mechanistic integrative computational model of macrophage polarization: Implications in human pathophysiology.PLoS computational biology · 2019Article
- IL-1β and TNFα Differentially Influence NF-κB Activity and FasL-Induced Apoptosis in Primary Murine Hepatocytes During LPS-Induced Inflammation.Frontiers in physiology · 2019Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophages are cells with remarkable plasticity. They integrate signals from their microenvironment leading to context-dependent polarization into classically (M1) or alternatively (M2) activated macrophages, representing two extremes of a broad spectrum of divergent phenotypes. Thereby, macrophages deliver protective and pro-regenerative signals towards injured tissue but, depending on the eliciting damage, may also be responsible for the generation and aggravation of tissue injury. Although incompletely understood, there is emerging evidence that macrophage polarization is critical for these antagonistic roles. To identify activation-specific expression patterns of chemokines and cytokines that may confer these distinct effects a systems biology approach was applied. A comprehensive literature-based Boolean model was developed to describe the M1 (LPS-activated) and M2 (IL-4/13-activated) polarization types. The model was validated using high-throughput transcript expression data from murine bone marrow derived macrophages. By dynamic modeling of gene expression, the chronology of pathway activation and autocrine signaling was estimated. Our results provide a deepened understanding of the physiological balance leading to M1/M2 activation, indicating the relevance of co-regulatory signals at the level of Akt1 or Akt2 that may be important for directing macrophage polarization.
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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.