ArticleHistology and histopathology2025
USP33 promotes pulmonary microvascular endothelial cell pyroptosis by stabilizing TRAF2 through deubiquitination.
Article in Histology and histopathology, 2025. 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
objectiveInhibiting the pyroptosis of human pulmonary microvascular endothelial cells (HPMECs) is a promising therapeutic modality for acute lung injury (ALI). Given the undefined effect of ubiquitin-specific protease 33 (USP33) and tumor necrosis factor receptor-associated factor 2 (TRAF2) on pyroptosis in lung injury, this study investigates their roles in the pyroptosis of HPMECs during ALI.
methodsThe hypoxia/reoxygenation (H/R)-induced model was constructed in HPMECs. Cell viability, cytotoxicity, and cell death were determined by the cell counting kit-8 (CCK-8), Lactate dehydrogenase (LDH), and Hoechst-PI staining, respectively. Western blot and qRT-PCR were used to detect protein and gene expression levels of pyroptosis-related markers, respectively. The TRAF2 ubiquitination level was measured via immunoprecipitation.
resultsUSP33 and TRAF2 expressions were elevated in H/R-induced HPMECs. Knockdown of USP33 increased cell viability and inhibited cellular pyroptosis, accompanied by decreases in IL-1β, IL-18, and Caspase-1. USP33 stabilized TRAF2 by deubiquitination. TRAF2 overexpression reversed the effect of USP33 silencing on suppressing HPMEC pyroptosis.
conclusionUSP33 stabilizes TRAF2 by deubiquitination to promote HPMEC pyroptosis during ALI.
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