ArticleFrontiers in aging neuroscience2016
Thromboxane A2 Receptor Stimulation Enhances Microglial Interleukin-1β and NO Biosynthesis Mediated by the Activation of ERK Pathway.
Article in Frontiers in aging neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 38 citations in OpenAlex.
- Insights into the Expression, Structure, and Function of the Thromboxane AACS pharmacology & translational science · 2025Review
- Acute effect of statins on vascular reactivity in maternal and placental arteries from pregnancies complicated by preeclampsia.Frontiers in physiology · 2025Article
- Article
- High Levels of Thromboxane (TX) Are Associated with the Sex-Dependent Non-Dipping Phenomenon in Ischemic Stroke Patients.Journal of clinical medicine · 2022Article
- G-Protein-Coupled Receptors and Ischemic Stroke: a Focus on Molecular Function and Therapeutic Potential.Molecular neurobiology · 2021Review
- Small molecules targeting cyclooxygenase/prostanoid cascade in experimental brain ischemia: Do they translate?Medicinal research reviews · 2021Review
- Pre- and Neonatal Exposure to Lead (Pb) Induces Neuroinflammation in the Forebrain Cortex, Hippocampus and Cerebellum of Rat Pups.International journal of molecular sciences · 2020Article
- Mechanism of tanshinones and phenolic acids from Danshen in the treatment of coronary heart disease based on co-expression network.BMC complementary medicine and therapies · 2020Article
- Idebenone Alleviates Neuroinflammation and Modulates Microglial Polarization in LPS-Stimulated BV2 Cells and MPTP-Induced Parkinson's Disease Mice.Frontiers in cellular neuroscience · 2018Article
- Thromboxane A2 receptor antagonist SQ29548 suppresses the LPS‑induced release of inflammatory cytokines in BV2 microglia cells via suppressing MAPK and NF‑κB signaling pathways.Molecular medicine reports · 2017Article
- Follistatin-like protein 1 suppressed pro-inflammatory cytokines expression during neuroinflammation induced by lipopolysaccharide.Journal of molecular histology · 2017Article
- Thromboxane A2 receptor antagonist SQ29548 reduces ischemic stroke-induced microglia/macrophages activation and enrichment, and ameliorates brain injury.Scientific reports · 2016Article
- Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeThromboxane A2 (TXA2) receptors (TP) interact with the ligand TXA2 to induce platelet aggregation and regulate hemostasis. Recently TP-mediated signaling has been suggested to function in multiple cell types in the brain. In this report, we aim to study the expression and physiological role of TP in microglia, in particular after brain ischemia.
methodsIschemic brain sections were analyzed for TP expression. Microglial cell line and primary microglia were cultured, or neuronal cell line co-culture system was used to determine the TP mediated signaling in inflammation and microglia activation.
resultsWe found that the TP level was significantly increased in ipsilateral mouse brain tissue at 24 h after ischemia-reperfusion, which was also found to partly co-localize with CD11b, a marker for microglial and infiltrated monocyte/macrophage, in peri-infarct area. Immunofluorescence staining of primary microglia and microglial cell line BV2 revealed the predominant membrane distribution of TP. Conditioned culture media from TP agonist U46619-treated BV2 cells decreased neuronal SH-SY5Y cell viability and induced apoptotic morphological changes. Furthermore, U46619 enhanced IL-1β, IL-6, and iNOS mRNA expression as well as IL-1β and NO releases in BV2 cells or primary microglia. Such stimulation could be attenuated by TP antagonist SQ29548 or MEK inhibitor U0126. The dose- and time-dependent extracellular-signal-regulated kinase (ERK) phosphorylation induced by U46619 further demonstrated ERK signaling-mediated microglia activation by TP agonist.
conclusionThis study has shown a novel role of TP in microglia activation via the ERK signaling pathway, which provides insights for the management of neuroinflammation in diseases like cerebral infarction.
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