ArticleJournal of leukocyte biology2011
Calcium/calmodulin-dependent protein kinase (CaMK) Ialpha mediates the macrophage inflammatory response to sepsis.
Article in Journal of leukocyte biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 57 citations in OpenAlex.
- Blue Light Enhances Bacterial Clearance and Reduces Organ Injury During Sepsis.Critical care medicine · 2018Trial
- Amelioration of gentamicin-induced acute kidney injury by trifluoperazine: in vivo mechanistic insights.Scientific reports · 2026Article
- Association between corrected serum calcium levels and 28-day mortality in patients with sepsis: A cohort study.Medicine · 2026Article
- Challenge Specific Modulation of Responses to Adjuvant-Induced Innate Immune Memory.Immunology · 2026Article
- Machine learning-driven identification and experimental validation of key biomarkers in the bile acid metabolic pathway associated with ulcerative colitis.Frontiers in immunology · 2026Article
- Cannabidiol and Alzheimer Disease: A Comprehensive Review and In Silico Insights Into Molecular Interactions.The European journal of neuroscience · 2025Review
- Sepsis restructures the mitochondrial calcium uniporter complex in the lymphoid tissues of mice and humans.Communications biology · 2025Article
- Association between plasma proteome and pulmonary heart disease: A two-stage Mendelian randomization analysis.The clinical respiratory journal · 2024Article
- Depletion of creatine phosphagen energetics with a covalent creatine kinase inhibitor.Nature chemical biology · 2023Article
- Molecular Mechanisms Underlying CaInternational journal of molecular sciences · 2022Review
- Article
- CaMKIV regulates mitochondrial dynamics during sepsis.Cell calcium · 2020Article
- High-Mobility Group Box 1 Protein Signaling in Painful Diabetic Neuropathy.International journal of molecular sciences · 2020Article
- Polymorphisms in CAMKK2 associate with susceptibility to sensory neuropathy in HIV patients treated without stavudine.Journal of neurovirology · 2019Article
- Proteomics in gastroparesis: unique and overlapping protein signatures in diabetic and idiopathic gastroparesis.American journal of physiology. Gastrointestinal and liver physiology · 2019Article
- Repositioning of the antipsychotic drug TFP for sepsis treatment.Journal of molecular medicine (Berlin, Germany) · 2019Article
- Macrophage-derived HMGB1 as a Pain Mediator in the Early Stage of Acute Pancreatitis in Mice: Targeting RAGE and CXCL12/CXCR4 Axis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2017Article
- Calcium/calmodulin-dependent protein kinase regulates the PINK1/Parkin and DJ-1 pathways of mitophagy during sepsis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Zinc Modulates Endotoxin-Induced Human Macrophage Inflammation through ZIP8 Induction and C/EBPβ Inhibition.PloS one · 2017Article
- Use of Biotelemetry to Define Physiology-Based Deterioration Thresholds in a Murine Cecal Ligation and Puncture Model of Sepsis.Critical care medicine · 2016Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Dysregulated Ca(2+) handling is prevalent during sepsis and postulated to perpetuate the aberrant inflammation underlying subsequent organ dysfunction and death. The signal transduction cascades mediating these processes are unknown. Here, we identify that CaMKIα mediates the Mϕ response to LPS in vitro and the inflammation and organ dysfunction of sepsis in vivo. We show that LPS induced active pThr(177)-CaMKIα in RAW 264.7 cells and murine peritoneal Mϕ, which if inhibited biochemically with STO609 (CaMKK inhibitor) or by RNAi, reduces LPS-induced production of IL-10. Transfection of constitutively active CaMKIα (CaMKI293), but not a kinase-deficient mutant (CaMKI293(K49A)), induces IL-10 release. This production of IL-10 is mediated by CaMKIα-dependent regulation of p38 MAPK activation. CaMKIα activity also mediates the cellular release of HMGB1 by colocalizing with and regulating the packaging of HMGB1 into secretory lysosomes. During endotoxemia, mice receiving in vivo CaMKIα(RNAi) display reduced systemic concentrations of IL-10 and HMGB1 in comparison with mice receiving NT(RNAi). These data support the biological relevance of CaMKIα-dependent IL-10 production and HMGB1 secretion. In a CLP model of sepsis, CaMKIα(RNAi) mice display reduced systemic concentrations of IL-10, IL-6, TNF-α, and HMGB1 in comparison with NT(RNAi) mice, which correlate with reductions in the development of renal dysfunction. These data support that CaMKIα signaling is integral to the Mϕ responding to LPS and may also be operant in vivo in regulating the inflammation and organ dysfunction consequent to sepsis.
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Registered trials
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