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• W4210273722 abstract "Excessive inflammatory activities are reported to be the primary cause of sepsis-induced acute kidney injury (AKI). Ras guanyl nucleotide-releasing protein (RasGRP) could prevent inflammatory response. However, its role in the regulation of inflammatory response in sepsis-associated AKI remains unclear.Wild-type or RasGRP1-deficient mice were treated with lipopolysaccharide intraperitoneally in combination with D-galactosamine to establish a mouse model of sepsis-associated AKI. Serum inflammatory cytokines were measured using enzyme-linked immunosorbent assay. The messenger RNA (mRNA) levels of interleukin 6, tumor necrosis factor, nitric oxide synthase 2, and interleukin 1β were measured using quantitative reverse-transcription polymerase chain reaction. The morphological change in kidney tubule was determined by hematoxylin-and-eosin staining. The protein levels of RasGRP, extracellular signal-regulated kinases 1 and 2 (ERK1/2), and c-Jun N-terminal kinase (JNK) were determined using Western blot.RasGRP1 mRNA and protein levels were significantly increased in patients with sepsis-related AKI compared to those in healthy subjects. RasGRP knockout markedly reduced inflammatory cytokines induced by AKI in sepsis when compared with wild-type mice. Additionally, RasGRP deficiency inhibited the phosphorylation of ERK1/2 without altering JNK expression. In conclusion, we demonstrate that RasGRP1 plays a pivotal role in sepsis-associated AKI. Downregulation of RasGRP1 could significantly inhibit inflammatory response by inhibiting the activation of ERK1/2 and mitogen-activated protein kinase pathway, thereby reducing AKI induced by sepsis.Our data suggest that RasGRP exacerbates lipopolysaccharide-induced acute kidney injury through regulating ERK activation, which reveals a potential therapeutic target for the treatment of sepsis-induced AKI." @default.
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• W4210273722 date "2022-01-31" @default.
• W4210273722 modified "2023-09-26" @default.
• W4210273722 title "RasGRP Exacerbates Lipopolysaccharide-Induced Acute Kidney Injury Through Regulation of ERK Activation" @default.
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• W4210273722 doi "https://doi.org/10.1093/ofid/ofac041" @default.
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