MerTK signaling in macrophages promotes the synthesis of inflammation resolution mediators by suppressing CaMKII activity
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concentration and suppressed the activity of calcium/calmodulin-dependent protein kinase II (CaMKII). This, in turn, reduced the activities of the mitogen-activated protein kinase (MAPK) p38 and the kinase MK2, resulting in the increased abundance of the nonphosphorylated, cytoplasmic form of 5-LOX and enhanced SPM biosynthesis. In a zymosan-induced peritonitis model, an inflammatory setting in which macrophage MerTK activation promotes resolution, inhibition of ERK activation delayed resolution, which was characterized by an increased number of neutrophils and decreased amounts of SPMs in tissue exudates. These findings contribute to our understanding of how MerTK signaling induces 5-LOX-derived SPM biosynthesis and suggest a therapeutic strategy to boost inflammation resolution in settings where defective resolution promotes disease progression.
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Similar effects were observed in response to dying cells in macrophages lacking Rac1 or the efferocytosis receptors merTK and TIM4.
“Similar effects were observed in response to dying cells in macrophages lacking Rac1 or the efferocytosis receptors merTK and TIM4 (Cai et al., 2018; Camenisch et al., 1999; Martinez et al., 2011; Scott et al., 2001; Thorp et al., 2008), consistent with this idea.”
From LC3-Associated Endocytosis Facilitates β-Amyloid Clearance and Mitigates Neurodegeneration in Murine Alzheimer’s Disease (2019) · cites this paper as Cai et al., 2018
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References 77 · Cited by 175
- Authors
- Cai, B., Kasikara, C., Doran, A. C., Ramakrishnan, R., Birge, R. B., & Tabas, I.
- Affiliations
- Columbia University (US)
- Rutgers, The State University of New Jersey (US)
- Corresponding author
- Cai, Bishuang
- Tabas, Ira
- Venue
- Science Signaling
- Published
- 2018-09-25
- Volume
- 11
- Issue
- 549
- ISSN
- 1937-9145 (ISSN-L)
- 1945-0877
- PMC
- PMC6171110
- OpenAlex
- W2893194863
- Cited by
- 175
- References
- 77
- Citations by year
- 2026: 29 · 2025: 26 · 2024: 21 · 2023: 19 · 2022: 23 · 2021: 34 · 2020: 12 · 2019: 11
- FWCI
- 11.74
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science Signaling (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Rutgers University Community Repository (Rutgers University) (submittedVersion)
- Figshare (submittedVersion, cc-by)
- Health Research Alliance (cc-by)
- Funders
- National Institutes of Health (HL132412)
- Topics
- Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Health Sciences › Medicine › Pharmacology › Inflammatory mediators and NSAID effects
- Keywords
- macrophages, inflammation resolution, CaMKII, 5-lipoxygenase, resolvins, p38 MAPK, ERK, zymosan-induced peritonitis, neutrophils
- MeSH terms
- c-Mer Tyrosine Kinase, Growth Arrest-Specific Protein 6, Animals, Arachidonate 5-Lipoxygenase, Calcium, Cytoplasm, Cytosol, Enzyme Activation, Humans, Inflammation, Macrophages, Mice, Inbred C57BL, Monocytes, Neutrophils, Peritonitis, Phosphorylation, Signal Transduction, Gene Expression Regulation, Enzymologic, Inflammation Mediators, Jurkat Cells, Intercellular Signaling Peptides and Proteins, Extracellular Signal-Regulated MAP Kinases, Mice, Sarcoplasmic Reticulum Calcium-Transporting ATPases, Calcium-Calmodulin-Dependent Protein Kinase Type 2, HEK293 Cells
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