ArticleInternational journal of molecular medicine2017
Crosstalk between TLR2 and Sphk1 in microglia in the cerebral ischemia/reperfusion-induced inflammatory response.
Article in International journal of molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 33 citations in OpenAlex.
- Identification and validation of microglia-associated genes in ischemic stroke using single-cell and bulk RNA-seq.Molecular brain · 2025Article
- Signaling controversy and future therapeutical perspectives of targeting sphingolipid network in cancer immune editing and resistance to tumor necrosis factor-α immunotherapy.Cell communication and signaling : CCS · 2024Review
- Th17 Cells and IL-17A in Ischemic Stroke.Molecular neurobiology · 2024Review
- Single-cell RNA sequencing reveals roles of unique retinal microglia types in early diabetic retinopathy.Diabetology & metabolic syndrome · 2024Article
- A narrative review of long noncoding RNA: insight into neural ischemia/reperfusion mediated by two pathophysiological processes of injury and repair.Annals of translational medicine · 2022Review
- Identification of TLR2 as a Key Target in Neuroinflammation in Vascular Dementia.Frontiers in genetics · 2022Article
- Dihydromyricetin Attenuates Cerebral Ischemia Reperfusion Injury by Inhibiting SPHK1/mTOR Signaling and Targeting Ferroptosis.Drug design, development and therapy · 2022Article
- miR-19a/b-3p promotes inflammation during cerebral ischemia/reperfusion injury via SIRT1/FoxO3/SPHK1 pathway.Journal of neuroinflammation · 2021Article
- Anti-IL-23 exerted protective effects on cerebral ischemia-reperfusion injury through JAK2/STAT3 signaling pathway.Molecular biology reports · 2021Article
- Sphingosine 1-Phosphate Receptors in Cerebral Ischemia.Neuromolecular medicine · 2021Review
- Comprehensive Landscape of Immune Infiltration and Aberrant Pathway Activation in Ischemic Stroke.Frontiers in immunology · 2021Article
- Transcriptomic Profiling Reveals the Antiapoptosis and Antioxidant Stress Effects ofFrontiers in neurology · 2021Article
- TLR2 antagonism attenuates the hippocampal neuronal damage in a murine model of sleep apnea via inhibiting neuroinflammation and oxidative stress.Sleep & breathing = Schlaf & Atmung · 2020Article
- Review
- Inhibition of microglial receptor-interacting protein kinase 1 ameliorates neuroinflammation following cerebral ischaemic stroke.Journal of cellular and molecular medicine · 2020Article
- The Intra-nuclear SphK2-S1P Axis Facilitates M1-to-M2 Shift of Microglia via Suppressing HDAC1-Mediated KLF4 Deacetylation.Frontiers in immunology · 2019Article
- Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stroke is associated with high morbidity and mortality, and much remains unknown about the injury-related mechanisms that occur following reperfusion. This study aimed to explore the roles of Toll-like receptor 2 (TLR2) and sphingosine kinase 1 (Sphk1) in microglial cells in inflammatory responses induced by cerebral ischemia/reperfusion (I/R). For this purpose, C57BL/6 mice were randomly divided into 4 groups as follows: the sham-operated group, the I/R group, the I/R group treated with TLR2 antibody, and the I/R group treated with N,N-dimethylsphingosine. Focal cerebral I/R was induced by middle cerebral artery occlusion. Double-labeling immunofluorescence was used to observe the protein expression of TLR2 and Sphk1 in the ischemic brain tissue. Quantitative polymerase chain reaction was performed to determine the mRNA levels of TLR2 and Sphkl in ischemic brain tissue. Enzyme-linked immunosorbent assay was carried out to detect the protein contents of interleukin (IL)-1β, tumor necrosis factor-α (TNF‑α), IL-17 and IL-23 in ischemic brain tissue. The results revealed that I/R upregulated TLR2 and Sphk1 expression in microglial cells, and the inhibition of either TLR2 or Sphk1 inhibited the expression of the pro-inflammatory cytokines, IL-1β, TNF-α, IL-17 and IL-23. Notably, the inhibition of TLR2 activity also decreased Sphk1 expression. These results thus indicate that the activation of microglial cells, via a TLR2→Sphk1→pro-inflammatory cytokine (IL-1β, TNF-α, IL-17 and IL-23) pathway, may participate in I/R injury.
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