ArticleExperimental & molecular medicine2014
β1-integrin-dependent migration of microglia in response to neuron-released α-synuclein.
Article in Experimental & molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 56 citations in OpenAlex.
- Microglia-Neuron Crosstalk: An Intimate Molecular Conversation in Neurodegeneration.International journal of molecular sciences · 2026Review
- Differential microglial responses to structurally distinct alpha-synuclein polymorphs.Molecular brain · 2025Article
- Redirecting microglia phenotype via inhibition of NFAT1 ameliorates deficits in mouse model of synucleinopathies.Experimental & molecular medicine · 2025Article
- Making tracks: microglia and the extracellular matrix.Molecular neurodegeneration · 2025Review
- Suppressing ROS Production of AIE Nanoprobes by Simple Matrices Optimization for CNS Cell Observation and Minimized Influence of Cytoskeleton Morphology.Chemical & biomedical imaging · 2024Article
- Lactylation-driven FTO targets CDK2 to aggravate microvascular anomalies in diabetic retinopathy.EMBO molecular medicine · 2024Article
- TREM2 is down-regulated by HSV1 in microglia and involved in antiviral defense in the brain.Science advances · 2023Article
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- Neuroprotective Effect of α-Lipoic Acid against AβMolecules (Basel, Switzerland) · 2023Article
- Involvement of TLR2-TLR4, NLRP3, and IL-17 in pain induced by a novel Sprague-Dawley rat model of experimental autoimmune encephalomyelitis.Frontiers in pain research (Lausanne, Switzerland) · 2022Article
- Neuromechanobiology: An Expanding Field Driven by the Force of Greater Focus.Advanced healthcare materials · 2021Review
- Article
- Periphery and brain, innate and adaptive immunity in Parkinson's disease.Acta neuropathologica · 2021Review
- Toll-like receptor 2 and 4 antagonism for the treatment of experimental autoimmune encephalomyelitis (EAE)-related pain.Brain, behavior, and immunity · 2021Article
- Effects of innate immune receptor stimulation on extracellular α-synuclein uptake and degradation by brain resident cells.Experimental & molecular medicine · 2021Article
- LRRK2 mediates microglial neurotoxicity via NFATc2 in rodent models of synucleinopathies.Science translational medicine · 2020Article
- CXCL12 is involved in α-synuclein-triggered neuroinflammation of Parkinson's disease.Journal of neuroinflammation · 2019Article
- Targeting Microglial and Neuronal Toll-like Receptor 2 in Synucleinopathies.Experimental neurobiology · 2019Review
- Alpha synuclein in hematopoiesis and immunity.Heliyon · 2019Review
- Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic neuroinflammation is an integral pathological feature of major neurodegenerative diseases. The recruitment of microglia to affected brain regions and the activation of these cells are the major events leading to disease-associated neuroinflammation. In a previous study, we showed that neuron-released α-synuclein can activate microglia through activating the Toll-like receptor 2 (TLR2) pathway, resulting in proinflammatory responses. However, it is not clear whether other signaling pathways are involved in the migration and activation of microglia in response to neuron-released α-synuclein. In the current study, we demonstrated that TLR2 activation is not sufficient for all of the changes manifested by microglia in response to neuron-released α-synuclein. Specifically, the migration of and morphological changes in microglia, triggered by neuron-released α-synuclein, did not require the activation of TLR2, whereas increased proliferation and production of cytokines were strictly under the control of TLR2. Construction of a hypothetical signaling network using computational tools and experimental validation with various peptide inhibitors showed that β1-integrin was necessary for both the morphological changes and the migration. However, neither proliferation nor cytokine production by microglia was dependent on the activation of β1-integrin. These results suggest that β1-integrin signaling is specifically responsible for the recruitment of microglia to the disease-affected brain regions, where neurons most likely release relatively high levels of α-synuclein.
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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.