ArticleJournal of neuroinflammation2018
Hippocampal CA1 βCaMKII mediates neuroinflammatory responses via COX-2/PGE2 signaling pathways in depression.
Article in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 2 of them syntheses that pooled it.
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Who cites it
70 citing papers in PubMed, 2 syntheses or guidelines pooled it, 121 citations in OpenAlex.
- The antidepressive mechanism of Longya Lilium combined with Fluoxetine in mice with depression-like behaviors.NPJ systems biology and applications · 2024Pooled it
- Assessment of bidirectional relationships between depression and rheumatoid arthritis among adults: a two-sample Mendelian randomization study.Clinical rheumatology · 2023Pooled it
- PACSIN2-mediated synaptic injury contributes to behavioral disorders caused by chronic stress.Acta pharmacologica Sinica · 2026Article
- Estrogen Replacement Therapy in Ovariectomized Rats: Complementary Roles of ER and GPR30 in Alleviating Depressive-like Behavior.Current issues in molecular biology · 2026Article
- Boldine Mitigates Chronic Unpredictable Stress-Induced Depression by Suppressing Serotonin 3A Receptor-Calcium/Calmodulin-Dependent Protein Kinase II Signaling and Nucleotide-Binding Domain Leucine-Rich Repeat Protein 3 Inflammasome in the Hippocampus.ACS pharmacology & translational science · 2026Article
- Metabolic profiling reveals potential biomarkers and underlying signaling pathways involved in mindfulness-based cognitive therapy-improved adolescent depression symptoms.EXCLI journal · 2026Article
- SS-31 improves post-cardiac arrest brain injury by inhibiting microglial ferroptosis and polarization.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Structural dynamics of mixed-subunit CaMKIIα/β heterododecamers filmed by high-speed AFM.Nature communications · 2025Article
- The role of arachidonic acid metabolites in major depressive disorder: mechanisms and therapeutic implications.Metabolic brain disease · 2025Review
- Dietary Acrylamide Induces Depression viaCurrent issues in molecular biology · 2025Article
- Regulating the Plasticity of Hippocampal Neurons via Electroacupuncture in Depression Model Mice.Cell proliferation · 2025Article
- CD38 connects the heart and brain.Translational psychiatry · 2025Review
- Implicating neuroinflammation in hippocampus, prefrontal cortex and amygdala with cognitive deficit: a narrative review.3 Biotech · 2025Review
- Ghrelin Inhibits Inflammasomes Activation in Astrocytes, Alleviates Pyroptosis, and Prevents Lipopolysaccharide-induced Depression-like Behavior in Mice.Inflammation · 2025Article
- Molecular Mechanisms Underlying Apple Extract Ameliorates Depression-Incident Cognitive Dysfunction Based on Network Pharmacology.Food science & nutrition · 2025Article
- Neuroinflammation-A Crucial Factor in the Pathophysiology of Depression-A Comprehensive Review.Biomolecules · 2025Review
- The Impact of Prevotella on Neurobiology in Aging: Deciphering Dendritic Cell Activity and Inflammatory Dynamics.Molecular neurobiology · 2024Review
- Acupuncture may play a key role in anti-depression through various mechanisms in depression.Chinese medicine · 2024Review
- An Analysis of the Intestinal Microbiome Combined with Metabolomics to Explore the Mechanism of How Jasmine Tea Improves Depression in CUMS-Treated Rats.Foods (Basel, Switzerland) · 2024Article
- Article
10 more citing papers are in PubMed but not listed here.
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6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundNeuroinflammation has recently emerged as a critical risk factor in the pathophysiology of depression. However, the underlying molecular mechanisms and the development of novel therapeutic strategies as means to target these inflammatory pathways for use in the treatment of depression remain unresolved. In the present study, we aimed to investigate the molecular events of neuroinflammation as related to its induction of depression-like behaviors.
methodsChronic unpredictable mild stress (CUMS) or lipopolysaccharide (LPS) was used to induce depression-like behaviors in rats. The inflammatory factors and related proteins were verified by RT-PCR, immunoblotting, and immunofluorescence assay. In vivo intracerebral injection of adenovirus-associated virus (AAV) in rats was used to overexpress or block the function of the β form of the calcium/calmodulin-dependent protein kinase type II (βCaMKII). In vivo intracerebroventricular injection of SB203580 was used to block p38 mitogen-activated protein kinase (MAPK). Finally, the prostaglandin E2 (PGE2) concentration was verified by using enzyme-linked assay kit.
resultsThe expression of cyclo-oxygenase (COX)-2, which is responsible for production of the pro-inflammatory factor PGE2 and thus glial activation, was increased in the CA1 hippocampus in a rat model of depression. Further, the βCaMKII in CA1 was significantly upregulated in depressed rats, while antidepressant treatment downregulated this kinase. Overexpression of βCaMKII via infusion of a constructed AAV-βCaMKII into the CA1 region resulted in phosphorylation of the p38 MAPK and the activating transcription factor 2 (ATF2). These effects were accompanied by an enhanced activity of the COX-2/PGE2 pathway and effectively induced core symptoms of depression. Conversely, knockdown of βCaMKII within the CA1 region reversed these inflammation-related biochemical parameters and significantly rescued depression symptoms.
conclusionThese results demonstrate that βCaMKII can act as a critical regulator in depression via activating neuroinflammatory pathways within the CA1 region. Moreover, this study provides new perspectives on molecular targets and drug therapies for future investigation in the treatment of depression.
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