Inflammatory cytokines enhance muscarinic-mediated arachidonic acid release through p38 mitogen-activated protein kinase in A2058 cells
Abstract
The human melanoma cell line A2058 expresses the Gq-coupled M5 subtype of muscarinic receptor. Stimulation with the cholinergic agonist, carbachol, induces a dose-dependent increase in arachidonic acid release. The carbachol-induced arachidonate release is potentiated two- to threefold by pretreatment of A2058 cells with either of the inflammatory cytokines, tumor necrosis factor-alpha or interleukin-1beta . Cytokine-induced enhancement of muscarinic-mediated arachidonic acid release peaks near 1 h. Western analysis suggests that both cytokines are capable of activating the nuclear factor-kappaB (NF-kappaB) and p38 mitogen-activated protein kinase (MAPK) pathways. Anisomycin (1 microM) treatment mimics the cytokine-induced enhancement of arachidonic acid production and activates the p38 MAPK pathway, but does not activate the NF-kappaB pathway. Furthermore, pre-treatment of A2058 cells with the putative p38 MAPK inhibitor, SB202190, ablates the cytokine-dependent augmentation without interfering with the muscarinic-mediated arachidonic acid release in untreated cells. Moreover, cytokine treatment does not affect other M5-coupled pathways (e.g., phospholipase C activity or intracellular Ca2+ mobilization), suggesting that p38 MAPK activation principally modulates muscarinic-mediated phospholipase A2 activity. Finally, in primary cultures of cells taken from rat cerebellum, key aspects of this finding are repeated in cultures enriched for glia, but not in cultures enriched for granule neurons.
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Muscarine, a positive regulator of PLA2, is a potent inducer of sAPPα in human neuroblastoma SH-SY5Y cells.
“It is interesting that muscarine, a positive regulator of PLA2, is also a potent inducer of sAPPα in human neuroblastoma SH-SY5Y cells (Webster et al., 2002; Wood et al., 2000);”
From Docosanoids and elovanoids from omega-3 fatty acids are pro-homeostatic modulators of inflammatory responses, cell damage and neuroprotection (2018) · cites this paper as Wood et al., 2000
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- Authors
- Wood, M. W., Segal, J. A., Mark, R. J., Ogden, A. M., & Felder, C. C.
- Affiliations
- Eli Lilly (United States) (US)
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2000-05
- Volume
- 74
- Issue
- 5
- Pages
- 2033-2040
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W2004265235
- Cited by
- 11
- References
- 45
- Citations by year
- 2022: 1 · 2018: 1 · 2013: 1
- FWCI
- 0.24
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
- Health Sciences › Medicine › Pharmacology › Inflammatory mediators and NSAID effects
- Keywords
- arachidonic acid release, p38 MAPK, inflammatory cytokines, TNF-α, IL-1β, nuclear factor-kappaB, phospholipase A2, carbachol, anisomycin, SB202190, Gq-coupled receptors
- MeSH terms
- Animals, Anisomycin, Carbachol, Cerebellum, Cerebral Cortex, Enzyme Activation, Enzyme Inhibitors, Humans, Imidazoles, Interleukin-1, Muscarine, Pyridines, Tumor Cells, Cultured, Tumor Necrosis Factor-alpha, Cytokines, NF-kappa B, Arachidonic Acid, Cholinergic Agonists, Inflammation Mediators, Mitogen-Activated Protein Kinases, p38 Mitogen-Activated Protein Kinases, Rats
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