ArticleJournal of neuroinflammation2019
JNK signalling mediates aspects of maternal immune activation: importance of maternal genotype in relation to schizophrenia risk.
Article in Journal of neuroinflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 41 citations in OpenAlex.
- The Molecular Machinery of Synaptic Plasticity and Its Potential Role in the Aetiology of Schizophrenia.Molecular neurobiology · 2026Review
- Nauclea officinalis extract rescues working memory deficits in adolescent maternal immune activation offspring by restoring cholinergic signaling.Frontiers in cell and developmental biology · 2026Article
- BRD4/MAP2K7/PGF Signaling Axis Promotes Senescence and Extracellular Matrix Metabolism of Nucleus Pulposus Cells in Intervertebral Disk Degeneration.Aging cell · 2025Article
- Comprehensive bioinformatics analysis identifies hub genes associated with immune cell infiltration in early-onset schizophrenia.BMC psychiatry · 2025Article
- Genetic analysis of the blood transcriptome of young healthy pigs to improve disease resilience.Genetics, selection, evolution : GSE · 2023Article
- Microglial cannabinoid receptor type 1 mediates social memory deficits in mice produced by adolescent THC exposure and 16p11.2 duplication.Nature communications · 2023Article
- Maternal immune activation and role of placenta in the prenatal programming of neurodevelopmental disorders.Neuronal signaling · 2023Review
- Investigating behavioral phenotypes related to autism spectrum disorder in a gene-environment interaction model ofFrontiers in neuroscience · 2023Article
- Differential Effects of Toll-Like Receptor Activation and Differential Mediation by MAP Kinases of Immune Responses in Microglial Cells.Cellular and molecular neurobiology · 2022Article
- Gene co-expression architecture in peripheral blood in a cohort of remitted first-episode schizophrenia patients.Schizophrenia (Heidelberg, Germany) · 2022Article
- LPS versus Poly I:C model: comparison of long-term effects of bacterial and viral maternal immune activation on the offspring.American journal of physiology. Regulatory, integrative and comparative physiology · 2022Review
- Distinct trans-placental effects of maternal immune activation by TLR3 and TLR7 agonists: implications for schizophrenia risk.Scientific reports · 2021Article
- Sex difference in the interrelationship between TNF-α and oxidative stress status in first-episode drug-naïve schizophrenia.Journal of neuroinflammation · 2021Article
- The poly(I:C)-induced maternal immune activation model; a systematic review and meta-analysis of cytokine levels in the offspring.Brain, behavior, & immunity - health · 2021Review
- JNK3 as Therapeutic Target and Biomarker in Neurodegenerative and Neurodevelopmental Brain Diseases.Cells · 2020Review
- Lasting and Sex-Dependent Impact of Maternal Immune Activation on Molecular Pathways of the Amygdala.Frontiers in neuroscience · 2020Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundImportant insight into the mechanisms through which gene-environmental interactions cause schizophrenia can be achieved through preclinical studies combining prenatal immune stimuli with disease-related genetic risk modifications. Accumulating evidence associates JNK signalling molecules, including MKK7/MAP2K7, with genetic risk. We tested the hypothesis that Map2k7 gene haploinsufficiency in mice would alter the prenatal immune response to the viral mimetic polyriboinosinic-polyribocytidylic acid (polyI:C), specifically investigating the impact of maternal versus foetal genetic variants.
methodsPolyI:C was administered to dams (E12.5), and cytokine/chemokine levels were measured 6 h later, in maternal plasma, placenta and embryonic brain.
resultsPolyI:C dramatically elevated maternal plasma levels of most cytokines/chemokines. Induction of IL-1β, IL-2, IL-10, IL-12, TNF-α and CXCL3 was enhanced, while CCL5 was suppressed, in Map2k7 hemizygous (Hz) dams relative to controls. Maternal polyI:C administration also increased embryonic brain chemokines, influenced by both maternal and embryonic genotype: CCL5 and CXCL10 levels were higher in embryonic brains from Map2k7 dams versus control dams; for CCL5, this was more pronounced in Map2k7 Hz embryos. Placental CXCL10 and CXCL12 levels were also elevated by polyI:C, the former enhanced and the latter suppressed, in placentae from maternal Map2k7 Hzs relative to control dams receiving polyI:C.
conclusionsThe results demonstrate JNK signalling as a mediator of MIA effects on the foetus. Since both elevated CXCL10 and supressed CXCL12 compromise developing GABAergic interneurons, the results support maternal immune challenge contributing to schizophrenia-associated neurodevelopmental abnormalities. The influence of Map2k7 on cytokine/chemokine induction converges the genetic and environmental aspects of schizophrenia, and the overt influence of maternal genotype offers an intriguing new insight into modulation of embryonic neurodevelopment by genetic risk.
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