ArticleJournal of neuroinflammation2016
1-Oleyl-lysophosphatidic acid (LPA) promotes polarization of BV-2 and primary murine microglia towards an M1-like phenotype.
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 64 papers.
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Who cites it
64 citing papers in PubMed, 115 citations in OpenAlex.
- Treatment of animal models of Alzheimer's disease with extracellular vesicles or exosomes and involvement of microRNAs.Neural regeneration research · 2026Article
- Lysophosphatidic Acid Receptor 5 (LPAInternational journal of molecular sciences · 2026Article
- Lysophosphatidic acid drives to mirror-image pain via corpus callosum-mediated propagation of inflammatory responses.Communications biology · 2026Article
- Polygonati Rhizoma Alleviates Vascular Dementia through Regulating Microglial Polarization Transitions Mediated by NF-κB/NLRP3 Pathway.Current pharmaceutical biotechnology · 2026Article
- Decoding lysophosphatidic acid signaling in physiology and disease: mapping the multimodal and multinodal signaling networks.Signal transduction and targeted therapy · 2025Review
- Unraveling the Role of Autotaxin and Lysophosphatidic Acid in Alzheimer's Disease: From Molecular Mechanisms to Therapeutic Potential.International journal of molecular sciences · 2025Review
- GIV/Girdin Modulation of Microglial Activation in Ischemic Stroke: Impact of FTO-Mediated m6A Modification.Molecular neurobiology · 2025Article
- CMPK2 promotes microglial activation through the cGAS-STING pathway in the neuroinflammatory mechanism.Scientific reports · 2025Article
- Non-saponin fromJournal of ginseng research · 2025Article
- Dolutegravir Derivatives Alleviate LPS-Induced Microglial Inflammation by Suppressing STAT1/3 Nuclear Translocation.Drug design, development and therapy · 2025Article
- MgSOFrontiers in nutrition · 2025Article
- Maresin-1 Ameliorates Sepsis-Induced Microglial Activation Through Modulation of the P38 MAPK Pathway.Neurochemical research · 2024Article
- Cordycepin Modulates Microglial M2 Polarization Coupled with Mitochondrial Metabolic Reprogramming by Targeting HKII and PDK2.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Tinosporae Radix attenuates acute pharyngitis by regulating glycerophospholipid metabolism and inflammatory responses through PI3K-Akt signaling pathway.Frontiers in pharmacology · 2024Article
- Vagus nerve stimulation: a physical therapy with promising potential for central nervous system disorders.Frontiers in neurology · 2024Review
- Lysophospholipid receptors in neurodegeneration and neuroprotection.Exploration of neuroprotective therapy · 2024Article
- Receptors on Microglia.Advances in neurobiology · 2024Review
- Reprimo (RPRM) as a Potential Preventive and Therapeutic Target for Radiation-Induced Brain Injury via Multiple Mechanisms.International journal of molecular sciences · 2023Article
- Regulation of oxygen-glucose deprivation/reperfusion-induced inflammatory responses and M1-M2 phenotype switch of BV2 microglia by lobetyolin.Metabolic brain disease · 2023Article
- Targeting Sigma-1 Receptor: A Promising Strategy in the Treatment of Parkinson's Disease.Neurochemical research · 2023Review
4 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundMicroglia, the immunocompetent cells of the CNS, rapidly respond to brain injury and disease by altering their morphology and phenotype to adopt an activated state. Microglia can exist broadly between two different states, namely the classical (M1) and the alternative (M2) phenotype. The first is characterized by the production of pro-inflammatory cytokines/chemokines and reactive oxygen and/or nitrogen species. In contrast, alternatively activated microglia are typified by an anti-inflammatory phenotype supporting wound healing and debris clearance. The objective of the present study was to determine the outcome of lysophosphatidic acid (LPA)-mediated signaling events on microglia polarization.
methodsLPA receptor expression and cyto-/chemokine mRNA levels in BV-2 and primary murine microglia (PMM) were determined by qPCR. M1/M2 marker expression was analyzed by Western blotting, immunofluorescence microscopy, or flow cytometry. Cyto-/chemokine secretion was quantitated by ELISA.
resultsBV-2 cells express LPA receptor 2 (LPA2), 3, 5, and 6, whereas PMM express LPA1, 2, 4, 5, and 6. We show that LPA treatment of BV-2 and PMM leads to a shift towards a pro-inflammatory M1-like phenotype. LPA treatment increased CD40 and CD86 (M1 markers) and reduced CD206 (M2 marker) expression. LPA increased inducible nitric oxide synthase (iNOS) and COX-2 levels (both M1), while the M2 marker Arginase-1 was suppressed in BV-2 cells. Immunofluorescence studies (iNOS, COX-2, Arginase-1, and RELMα) extended these findings to PMM. Upregulation of M1 markers in BV-2 and PMM was accompanied by increased cyto-/chemokine transcription and secretion (IL-1β, TNFα, IL-6, CCL5, and CXCL2). The pharmacological LPA5 antagonist TCLPA5 blunted most of these pro-inflammatory responses.
conclusionsLPA drives BV-2 and PMM towards a pro-inflammatory M1-like phenotype. Suppression by TCLPA5 indicates that the LPA/LPA5 signaling axis could represent a potential pharmacological target to interfere with microglia polarization in disease.
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