ArticleNeurochemical research2018
Complement Component C3 Promotes Cerebral Ischemia/Reperfusion Injury Mediated by TLR2/NFκB Activation in Diabetic Mice.
Article in Neurochemical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
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- TLR2 mediates renal apoptosis in neonatal mice subjected experimentally to obstructive nephropathy.PloS one · 2023Article
- Phosphoproteome Analysis Identifies a Synaptotagmin-1-Associated Complex Involved in Ischemic Neuron Injury.Molecular & cellular proteomics : MCP · 2022Article
- Therapeutic Potential of Mesenchymal Stem Cells (MSCs) and MSC-Derived Extracellular Vesicles for the Treatment of Spinal Cord Injury.International journal of molecular sciences · 2021Review
- High serum complement component C4 as a unique predictor of unfavorable outcomes in diabetic stroke.Metabolic brain disease · 2021Article
- Postconditioning attenuates myocardial ischemia-reperfusion injury by inhibiting complement activation and upregulation of miR-499.Experimental and therapeutic medicine · 2021Article
- C3 Deficiency Leads to Increased Angiogenesis and Elevated Pro-Angiogenic Leukocyte Recruitment in Ischemic Muscle Tissue.International journal of molecular sciences · 2021Article
- Minimizing Ischemia Reperfusion Injury in Xenotransplantation.Frontiers in immunology · 2021Review
- Screening of serum protein biomarkers in hemorrhagic cerebral infarction by surface-enhanced laser desorption/ionization time-of-flight mass spectrometry (SELDI-TOF-MS) technology.Annals of translational medicine · 2020Article
- Integrated analysis of the proteome and transcriptome in a MCAO mouse model revealed the molecular landscape during stroke progression.Journal of advanced research · 2020Article
- Changes of complement and oxidative stress parameters in patients with acute cerebral infarction or cerebral hemorrhage and the clinical significance.Experimental and therapeutic medicine · 2020Article
- Investigation of the underlying hub genes and mechanisms of reperfusion injury in patients undergoing coronary artery bypass graft surgery by integrated bioinformatic analyses.Annals of translational medicine · 2019Article
- The key genes, phosphoproteins, processes, and pathways affected by efavirenz-activated CYP46A1 in the amyloid-decreasing paradigm of efavirenz treatment.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Complement component C3 (C3), a key factor in the complement system, is heavily involved in various inflammation-associated diseases. However, it remains obscure for its role in the pathogenesis of cerebral ischemia/reperfusion (I/R) injury in diabetes. A transient middle cerebral artery occlusion (tMCAO) model was used for cerebral I/R injury in streptozotocin-induced diabetic mice. Cerebral infarct volume and neurological function were measured at different times of reperfusion. Complement C3 was measured by ELISA and western blotting. It was observed that complement C3 expression was increased in cerebral I/R injury of diabetic mice, whereas complement C3 deficiency abrogated the activation and injury. Furthermore, activating complement C3 promotes TLR2/NFκB activation after I/R injury in diabetic mice, which is inhibited by of the silencing of TLR2. Taken together, our data demonstrate that complement C3 promotes cerebral I/R injury via the TLR2/NFκB pathway in diabetic mice, and regulating the complement C3/TLR2/NFκB pathway may be a novel target for therapeutic intervention in diabetic stroke.
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