ArticleCell & bioscience2026
The ubiquitin E3 ligase TRIM59 in myeloid cell regulates complement C3 through degrading CCAAT/enhancer binding protein β to promote neuron survival after ischemic stroke.
Article in Cell & bioscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundIschemic stroke is a cerebrovascular disease that activates the complement system, leading to inflammation and neuronal injury. TRIM59, an E3 ubiquitin ligase, has been extensively studied in cancer, sepsis, and myocardial infarction, and is upregulated in macrophages after ischemic stroke. This study used myeloid cell Trim59 conditional knockout and macrophage-specific Trim59 overexpression mice to investigate the role of macrophage TRIM59 in regulating complement C3 release and neuronal phagocytosis following cerebral ischemia.
methodsMyeloid cell Trim59 conditional knockout (Trim59-cKO) mice were generated and bred using the Cre-loxP system, and macrophage-specific Trim59 overexpressing (AAV-Trim59) mice were constructed via intra-bone marrow injection. Middle cerebral artery occlusion/reperfusion (MCAO/R) and photothrombotic (PT) surgery were used to mimic the cerebral ischemia in mice. RT-qPCR, ELISA and immunofluorescence staining were performed to detect the expression of complement molecules and synaptic engulfment. Neurobehavioral tests were performed during recovery phase. Western blot and co-immunoprecipitation (Co-IP) assay were utilized to analyze the effect of TRIM59 on C3 expression and its transcription factor CCAAT/enhancer binding protein β (c/EBPβ).
resultsCompared to Trim59
conclusionMacrophage TRIM59 is critical for controlling excessive complement C3 activation, release, and phagocytosis after ischemic stroke by promoting ubiquitin-mediated degradation of its transcription factor c/EBPβ, providing a potential therapeutic target for cerebral ischemia.
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