ArticleJournal of neuroscience research2009
C1q, the recognition subcomponent of the classical pathway of complement, drives microglial activation.
Article in Journal of neuroscience research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
What it found
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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
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Who cites it
66 citing papers in PubMed, 115 citations in OpenAlex.
- C1q-CD44 interactions regulate microglial phagocytosis, proliferation, and migration.Journal of neuroinflammation · 2026Article
- The Interaction of Neutrophil Extracellular Traps and Complement in Intracerebral Hemorrhage.Cellular and molecular neurobiology · 2026Review
- Interaction Between Microglial Lipid Droplet Metabolism and Immune Polarisation After Stroke: Mechanisms and Therapeutic Prospects.Cellular and molecular neurobiology · 2025Review
- C1q-CD44 interactions regulate microglial phagocytosis, proliferation, and migration.Research square · 2025Article
- Astrocytic Hevin/SPARCL-1 Regulates Cognitive Decline in Pathological and Normal Brain Aging.Aging cell · 2025Article
- The E3 ligase c-Cbl modulates microglial phenotypes and contributes to Parkinson's disease pathology.Cell death discovery · 2025Article
- Cholesterol metabolism and neuroinflammatory changes in a non-human primate spinal nerve ligation model.Scientific reports · 2025Article
- Multidimensional analysis of matched primary and recurrent glioblastoma identifies contributors to tumor recurrence influencing time to relapse.Journal of neuropathology and experimental neurology · 2025Article
- Microglia-Astrocyte Crosstalk in Post-Stroke Neuroinflammation: Mechanisms and Therapeutic Strategies.Current neuropharmacology · 2025Review
- Short-term high fat diet impairs memory, exacerbates the neuroimmune response, and evokes synaptic degradation via a complement-dependent mechanism in a mouse model of Alzheimer's disease.Brain, behavior, and immunity · 2024Article
- Organelle phenotyping and multi-dimensional microscopy identify C1q as a novel regulator of microglial function.Journal of neurochemistry · 2024Article
- Complement in Human Brain Health: Potential of Dietary Food in Relation to Neurodegenerative Diseases.Foods (Basel, Switzerland) · 2023Review
- A single-cell transcriptional landscape of immune cells shows disease-specific changes of T cell and macrophage populations in human achalasia.Nature communications · 2023Article
- Candidate neuroinflammatory markers of cerebral autoregulation dysfunction in human acute brain injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Review
- Neuronal glutathione loss leads to neurodegeneration involving gasdermin activation.Scientific reports · 2023Article
- Complement: The Road Less Traveled.Journal of immunology (Baltimore, Md. : 1950) · 2023Review
- Tackling Neuroinflammation After Traumatic Brain Injury: Complement Inhibition as a Therapy for Secondary Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- Dietary fatty acids differentially impact phagocytosis, inflammatory gene expression, and mitochondrial respiration in microglial and neuronal cell models.Frontiers in cellular neuroscience · 2023Article
- C1q and central nervous system disorders.Frontiers in immunology · 2023Review
- Microglia in motor neuron disease: Signaling evidence from last 10 years.Developmental neurobiology · 2022Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Microglia, central nervous system (CNS) resident phagocytic cells, persistently police the integrity of CNS tissue and respond to any kind of damage or pathophysiological changes. These cells sense and rapidly respond to danger and inflammatory signals by changing their cell morphology; by release of cytokines, chemokines, or nitric oxide; and by changing their MHC expression profile. We have shown previously that microglial biosynthesis of the complement subcomponent C1q may serve as a reliable marker of microglial activation ranging from undetectable levels of C1q biosynthesis in resting microglia to abundant C1q expression in activated, nonramified microglia. In this study, we demonstrate that cultured microglial cells respond to extrinsic C1q with a marked intracellular Ca(2+) increase. A shift toward proinflammatory microglial activation is indicated by the release of interleukin-6, tumor necrosis factor-alpha, and nitric oxide and the oxidative burst in rat primary microglial cells, an activation and differentiation process similar to the proinflammatory response of microglia to exposure to lipopolysaccharide. Our findings indicate 1) that extrinsic plasma C1q is involved in the initiation of microglial activation in the course of CNS diseases with blood-brain barrier impairment and 2) that C1q synthesized and released by activated microglia is likely to contribute in an autocrine/paracrine way to maintain and balance microglial activation in the diseased CNS tissue.
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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.