ArticlePloS one2013
Deficiency in p38β MAPK fails to inhibit cytokine production or protect neurons against inflammatory insult in in vitro and in vivo mouse models.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Functions of p38 MAP Kinases in the Central Nervous System.Frontiers in molecular neuroscience · 2020Review
- Stress-Activated Protein Kinases in Spinal Cord Injury: Focus on Roles of p38.International journal of molecular sciences · 2018Review
- Molecular signaling underlying bulleyaconitine A (BAA)-induced microglial expression of prodynorphin.Scientific reports · 2017Article
- Phospholipase A2 of Peroxiredoxin 6 Plays a Critical Role in Cerebral Ischemia/Reperfusion Inflammatory Injury.Frontiers in cellular neuroscience · 2017Article
- p38 MAP kinases in the heart.Gene · 2016Review
- Inhibition of neuronal p38α, but not p38β MAPK, provides neuroprotection against three different neurotoxic insults.Journal of molecular neuroscience : MN · 2015Article
- Neuroinflammation in Alzheimer's disease.Neuropsychiatric disease and treatment · 2015Review
- The p38alpha mitogen-activated protein kinase limits the CNS proinflammatory cytokine response to systemic lipopolysaccharide, potentially through an IL-10 dependent mechanism.Journal of neuroinflammation · 2014Article
- Target engagement analysis and link to pharmacodynamic endpoint for a novel class of CNS-penetrant and efficacious p38α MAPK inhibitors.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2014Article
- Functional roles of p38 mitogen-activated protein kinase in macrophage-mediated inflammatory responses.Mediators of inflammation · 2014Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The p38 MAPK pathway plays a key role in regulating the production of proinflammatory cytokines, such as TNFα and IL-1β, in peripheral inflammatory disorders. There are four major isoforms of p38 MAPK (p38α, β, δ, γ), with p38α and p38β the targets of most p38 MAPK inhibitor drugs. Our previous studies demonstrated that the p38α MAPK isoform is an important contributor to stressor-induced proinflammatory cytokine up-regulation and neurotoxicity in the brain. However, the potential role of the p38β MAPK isoform in CNS proinflammatory cytokine overproduction and neurotoxicity is poorly understood. In the current studies, we used primary microglia from wild type (WT) and p38β knockout (KO) mice in co-culture with WT neurons, and measured proinflammatory cytokines and neuron death after LPS insult. We also measured neuroinflammatory responses in vivo in WT and p38β KO mice after administration of LPS by intraperitoneal or intracerebroventricular injection. WT and p38β KO microglia/neuron co-cultures showed similar levels of TNFα and IL-1β production in response to LPS treatment, and no differences in LPS-induced neurotoxicity. The in vitro results were confirmed in vivo, where levels of TNFα and IL-1β in the CNS were not significantly different between WT or p38β KO mice after LPS insult. Our results suggest that, similar to peripheral inflammation, p38α is critical but p38β MAPK is dispensable in the brain in regards to proinflammatory cytokine production and neurotoxicity induced by LPS inflammatory insult.
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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.