ArticleHereditas2025
Activation of TRAF1 induced by USP7/SP1 exacerbates the severity of infantile pneumonia.
Article in Hereditas, 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
backgroundInfantile pneumonia (IP) is a leading cause of morbidity and mortality in children worldwide, with limited treatment options. Tumor necrosis factor receptor-associated factor 1 (TRAF1) has been implicated in the pathogenesis of various inflammatory diseases. Given the lack of effective therapies in IP, understanding the role of TRAF1 in regulating IP is crucial for developing new therapeutic strategies.
methodsThis study utilized in vitro and in vivo models to investigate the role of TRAF1 in IP. WI-38 cells were stimulated with lipopolysaccharide (LPS), and rats were administered LPS to mimic IP. The mRNA expression of TRAF1 and Sp1 transcription factor (SP1) was analyzed using quantitative real-time polymerase chain reaction. The protein expression of TRAF1, ubiquitin-specific peptidase 7 (USP7), and SP1 was detected by western blotting. Cell viability and apoptosis were assessed using cell counting kit-8 assay and flow cytometry/TUNEL assays, respectively. Interleukin-6 and tumor necrosis factor-α levels were measured by enzyme-linked immunosorbent assays. Reactive oxygen species and malondialdehyde levels were analyzed using fluorescence microscopy and colorimetric assays. The interactions among USP7, TRAF1, and SP1 were identified using co-immunoprecipitation assay, immunofluorescence assay, and dual-luciferase reporter assay. TRAF1 silencing-induced effects were validated in a rat model. Lung tissue pathology was assessed using haematoxylin and eosin assay and Massion assay.
resultsLPS treatment induced apoptosis, inflammation, and oxidative stress of WI-38 cells, however, TRAF1 silencing ameliorated these effects. USP7 stabilized TRAF1 protein expression through its deubiquitinating activity, while TRAF1 overexpression reversed the effects of USP7 silencing in LPS-treated WI-38 cells. In addition, SP1 transcriptionally activated TRAF1 in WI-38 cells. Further, TRAF1 silencing improved lung injury in LPS-induced mice.
conclusionActivation of TRAF1 by USP7/SP1 exacerbated the severity of IP, suggesting that targeting TRAF1 may have significant clinical implications for the treatment of IP.
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