ArticleJournal of neuroinflammation2016
Activated brain mast cells contribute to postoperative cognitive dysfunction by evoking microglia activation and neuronal apoptosis.
Article in Journal of neuroinflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers, 1 of them a synthesis that pooled it.
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Who cites it
113 citing papers in PubMed, 1 synthesis or guideline pooled it, 193 citations in OpenAlex.
- Effect of dexmedetomidine on postoperative cognitive function in patients with gastrointestinal cancer: a meta-analysis of randomized controlled trials.Frontiers in neurologyPooled it
- Trial
- Adipose tissue plays a crucial role in obesity-induced postoperative neurocognitive disorders.Journal of translational medicine · 2026Article
- Article
- Chronic allergic lung inflammation is associated with brain mast cell-mediated suppression of neuronal activity and behavioral changes in mice.Respiratory research · 2026Article
- Thioredoxin-1 Regulates Microglia Polarization to Ameliorate Neuroinflammation and Cognitive Impairment Following Tumor-Therapeutic Ovariectomy.Endocrine, metabolic & immune disorders drug targets · 2026Article
- Disodium Cromoglycate Attenuates the Depressive-Like Behaviors in Mice by Inhibiting Neuroinflammation.CNS neuroscience & therapeutics · 2026Article
- Role of Esketamine in Attenuating Neuroinflammation and Improving Postoperative Cognitive Function via Autophagy Activation Through PARP1 Targeting.Physiological research · 2025Article
- Bidirectional Interplay Between Microglia and Mast Cells.International journal of molecular sciences · 2025Review
- Role of mast cell-derived exosomes in exacerbating neuronal injury of experimental cerebral malaria.Parasites & vectors · 2025Article
- Mast cell tryptase-PAR2 axis promotes ovarian fibrosis through RNF152-mediated stabilization of Bcl-xL.Journal of ovarian research · 2025Article
- Ulinastatin modulates TRPM4 expression and apoptosis to mitigate cognitive dysfunction in aged perioperative neurocognitive disorder rats.Scientific reports · 2025Article
- Recent Advances in the Mechanisms of Postoperative Neurocognitive Dysfunction: A Narrative Review.Biomedicines · 2025Review
- The therapeutic potential of glucagon-like peptide-1 receptor analogs for neuroinflammation in the setting of asthma.Exploration of asthma & allergy · 2025Article
- Role of TREM1 in the sevoflurane-induced inflammatory activation of microglia in vitro.Ibrain · 2025Article
- ICU patient-on-a-chip emulating orchestration of mast cells and cerebral organoids in neuroinflammation.Communications biology · 2024Article
- Postoperative Electroacupuncture Boosts Cognitive Function Recovery after Laparotomy in Mice.Biomolecules · 2024Article
- Article
- Mast Cells in Autism Spectrum Disorder-The Enigma to Be Solved?International journal of molecular sciences · 2024Review
- Peripheral inflammation as a potential mechanism and preventive strategy for perioperative neurocognitive disorder under general anesthesia and surgery.Frontiers in cellular neuroscience · 2024Review
53 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNeuroinflammation plays a key role in the occurrence and development of postoperative cognitive dysfunction (POCD). Microglia, the resident immune cells in the brain, has been increasingly recognized to contribute to neuroinflammation. Although brain mast cells (MCs) are the "first responder" in the brain injury rather than microglia, little is known about the functional aspects of MCs-microglia interactions.
methodsMale Sprague-Dawley (SD) rats were injected intracerebroventricular with MC stabilizer Cromolyn (100 μg/μl), MC stimulator C48/80 (1 μg/μl), or sterile saline 30 min before open tibial fracture surgery, and the levels of neuroinflammation and memory dysfunction were tested 1 and 3 days after surgery. In addition, the effect of activated MCs on microglia and neurons was determined in vitro.
resultsTibial fracture surgery induced MCs degranulation, microglia activation, and inflammatory factors production, which initiated the acute brain inflammatory response and neuronal death and exhibited cognitive deficit. Site-directed preinjection of the "MCs stabilizer" disodium cromoglycate (Cromolyn) inhibited this effect, including decrease of inflammatory cytokines, reduced MCs degranulation, microglia activation, neuronal death, and improved cognitive function 24 h after the surgery. In vitro study, we found that the conditioned medium from lipopolysaccharide (LPS)-stimulated mast cells line (P815) could induce primary microglia activation through mitogen-activated protein kinase (MAPK) pathway signaling and subsequent production of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). In addition, the activated P815 could directly induce neuronal apoptosis and synapse injury with microglia independently. Cromolyn could inhibit P815 activation following improved microglia activation and neuronal loss.
conclusionsThese results implicate that activated MCs could trigger microglia activation and neuronal damage, resulting in central nervous system (CNS) inflammation, and communications of MCs with microglia and neuron could constitute a new and unique therapeutic target for CNS immune inflammation-related diseases.
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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.