ArticleNeurotoxicity research2014
In vivo molecular markers for pro-inflammatory cytokine M1 stage and resident microglia in trimethyltin-induced hippocampal injury.
Article in Neurotoxicity research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- The Key Drivers of Brain Injury by Systemic Inflammatory Responses after Sepsis: Microglia and Neuroinflammation.Molecular neurobiology · 2023Pooled it
- Bloodstream Infection-induced Neuroinflammation: from Systemic Infection To Brain Invasion.Current microbiology · 2025Review
- The impact and mechanisms of YL-IPA08, a potent ligand for the translocator protein (18 kDa) on protection against LPS-induced depression and cognitive dysfunction in rodents.Metabolic brain disease · 2025Article
- β2 integrin regulates neutrophil trans endothelial migration following traumatic brain injury.Cell communication and signaling : CCS · 2025Article
- Neutrophils: a subgroup of neglected immune cells in ALS.Frontiers in immunology · 2023Review
- Brain-immune interaction mechanisms: Implications for cognitive dysfunction in psychiatric disorders.Cell proliferation · 2022Review
- Crosstalk between Microglia and Neurons in Neurotrauma: An Overview of the Underlying Mechanisms.Current neuropharmacology · 2022Review
- Isolation of microglia from retinas of chronic ocular hypertensive rats.Open life sciences · 2021Article
- Lipocalin-2 in Diabetic Complications of the Nervous System: Physiology, Pathology, and Beyond.Frontiers in physiology · 2021Review
- Microglia dynamics in adolescent traumatic brain injury.Journal of neuroinflammation · 2020Review
- An association between mitochondria and microglia effector function. What do we think we know?Neuroimmunology and neuroinflammation · 2020Article
- Neutrophils in traumatic brain injury (TBI): friend or foe?Journal of neuroinflammation · 2018Review
- Early Microglial Activation Following Closed-Head Concussive Injury Is Dominated by Pro-Inflammatory M-1 Type.Frontiers in neurology · 2018Article
- Vitamin D Treatment Attenuates Neuroinflammation and Dopaminergic Neurodegeneration in an Animal Model of Parkinson's Disease, Shifting M1 to M2 Microglia Responses.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2017Article
- The Pollutant Organotins Leads to Respiratory Disease by Inflammation: A Mini-Review.Frontiers in endocrinology · 2017Review
- Association Between Microglia, Inflammatory Factors, and Complement with Loss of Hippocampal Mossy Fiber Synapses Induced by Trimethyltin.Neurotoxicity research · 2016Article
- Blast exposure causes dynamic microglial/macrophage responses and microdomains of brain microvessel dysfunction.Neuroscience · 2016Article
- In Vitro Metabolomic Approach to Hippocampal Neurodegeneration Induced by Trimethyltin.Neurochemical research · 2016Article
- Microglial M1/M2 polarization and metabolic states.British journal of pharmacology · 2016Review
- Contributions of nonhematopoietic cells and mediators to immune responses: implications for immunotoxicology.Toxicological sciences : an official journal of the Society of Toxicology · 2015Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Microglia polarization to the classical M1 activation state is characterized by elevated pro-inflammatory cytokines; however, a full profile has not been generated in the early stages of a sterile inflammatory response recruiting only resident microglia. We characterized the initial M1 state in a hippocampal injury model dependent upon tumor necrosis factor (TNF) receptor signaling for dentate granule cell death. Twenty-one-day-old CD1 male mice were injected with trimethyltin (TMT 2.3 mg/kg, i.p.) and the hippocampus was examined at an early stage (24-h post-dosing) of neuronal death. Glia activation was assessed using a custom quantitative nuclease protection assay. We report elevated mRNA levels for glia response such as ionizing calcium-binding adapter molecule-1 and glial fibrillary acidic protein (Gfap); Fas, hypoxia inducible factor alpha, complement component 1qb, TNF-related genes (Tnf, Tnfaip3, Tnfrsfla); interleukin-1 alpha, Cd44, chemokine (C-C motif) ligand (Ccl)2, Cc14, integrin alpha M, lipocalin (Lcn2), and secreted phosphoprotein 1 (Spp1). These changes occurred in the absence of changes in matrix metalloproteinase 9 and 12, neural cell adhesion molecule, metabotropic glutamate receptor (Grm)3, and Ly6/neurotoxin 1 (Lynx1), as well as, a decrease in neurotrophin 3, glutamate receptor subunit epsilon (Grin)-2b, and neurotrophic tyrosine kinase receptor, type 3. The M2 anti-inflammatory marker, transforming growth factor beta-1 (Tgfb1) was elevated. mRNAs associated with early stage of injury-induced neurogenesis including fibroblast growth factor 21 and Mki67 were elevated. In the "non-injured" temporal cortex receiving projections from the hippocampus, Lynx1, Grm3, and Grin2b were decreased and Gfap increased. Formalin fixed-paraffin-embedded tissue did not generate a comparable profile.
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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.