ArticleNeurotoxicology2018
Characterization and comparative analysis of a new mouse microglial cell model for studying neuroinflammatory mechanisms during neurotoxic insults.
Article in Neurotoxicology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Microglia-Mediated Ependymal Injury in Bacille Calmette-Guérin-Induced Meningitis Is Attenuated by Sodium Butyrate with Restoration of Hmgcs2 Expression.Advances in respiratory medicine · 2026Article
- Mutant KRAS in brain endothelial cells promotes vascular inflammation and impairs vascular integrity in brain arteriovenous malformation.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Article
- Small Extracellular Vesicles from Neural Cells: Physiological and Pathological Roles, and Potential in Neurodegenerative Therapy.Advanced healthcare materials · 2026Review
- Protective Effects of Safranal Against Spike Protein-Induced Mitochondrial Dysfunction and Inflammation in Peripheral and Central Immune Cells.Current developments in nutrition · 2026Article
- SIRT1 deacetylates GAPDH to drive microglial glycolysis and neuroinflammation.Frontiers in immunology · 2026Article
- Subchronic oral toxicity and in vitro anti-neuroinflammatory evaluation ofToxicology reports · 2025Article
- Type 2 diabetes microenvironment promotes the development of Parkinson's disease by activating microglial cell inflammation.Frontiers in cell and developmental biology · 2024Article
- The RhoA-ROCK1/ROCK2 Pathway Exacerbates Inflammatory Signaling in Immortalized and Primary Microglia.Cells · 2023Article
- Microglial immune regulation by epigenetic reprogramming through histone H3K27 acetylation in neuroinflammation.Frontiers in immunology · 2023Article
- Deltamethrin-Evoked ER Stress Promotes Neuroinflammation in the Adult Mouse Hippocampus.Cells · 2022Article
- Isoginkgetin treatment attenuated lipopolysaccharide-induced monoamine neurotransmitter deficiency and depression-like behaviors through downregulating p38/NF-κB signaling pathway and suppressing microglia-induced apoptosis.Journal of psychopharmacology (Oxford, England) · 2021Article
- Unique molecular characteristics and microglial origin of Kv1.3 channel-positive brain myeloid cells in Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Phoenixin-20 Ameliorates Lipopolysaccharide-Induced Activation of Microglial NLRP3 Inflammasome.Neurotoxicity research · 2020Article
- Involvement of NFƙB and MAPK signaling pathways in the preventive effects of Ganoderma lucidum on the inflammation of BV-2 microglial cells induced by LPS.Journal of neuroimmunology · 2020Article
- Kv1.3 modulates neuroinflammation and neurodegeneration in Parkinson's disease.The Journal of clinical investigation · 2020Article
- Transcriptomic profile analysis of brain inferior colliculus following acute hydrogen sulfide exposure.Toxicology · 2020Article
- Molecular Signatures of Neuroinflammation Induced by αSynuclein Aggregates in Microglial Cells.Frontiers in immunology · 2020Article
- Fyn kinase regulates misfolded α-synuclein uptake and NLRP3 inflammasome activation in microglia.The Journal of experimental medicine · 2019Article
- Manganese activates NLRP3 inflammasome signaling and propagates exosomal release of ASC in microglial cells.Science signaling · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Microglia are the first responders of the central nervous system, acting as the key modulators of neuroinflammation observed during neurotoxic insults as well as in the pathophysiology of several neurodegenerative disorders including Alzheimer's (AD), Parkinson's (PD), and Huntington's diseases (HD). The number of publications on microglia has increased steadily throughout the past decade because of immense interests in the neuroinflammation that precedes the neurodegenerative process. To study microglial biology and its role in modulating neuroinflammation, immortalized microglial cell lines derived from mice, rats, and humans have been developed. Among these, the BV2 mouse microglial cell line is the most well characterized and widely used cell culture model. However, even unstimulated BV2 cells exhibit an amoeboid, hypertrophied morphology, indicating a highly activated and inflammatory state compared to primary microglia, thus making them less than ideal for studying the low-dose effects of toxicants on microglial activation. Therefore, we performed an in-depth characterization of a recently developed mouse microglial cell (MMC) line, which we compared with primary mouse microglia (PMG) and BV2s to identify which cell line was best suited for studying the microglial response to neurotoxicants. Comparative analyses reveal that MMCs are strikingly more similar to PMGs in basal activity, morphology, and sensitivity, than are BV2s. Furthermore, basal nitrite and inflammatory cytokine levels are significantly higher in BV2s compared to MMCs. BV2 cells are also less reactive to the inflammagen LPS compared to MMCs, due to the higher basal activation state of BV2s. Collectively, our in-depth analyses of morphology, basal activity, and responsivity to two different stimuli (LPS, aggregated α-synuclein) demonstrate that MMCs closely mimic neonatal PMGs, and are discernibly more suitable than BV2s for studying the neuroinflammatory mechanisms of neurotoxicants.
Indexed as
Identifiers
What OpenQuestion holds
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.