ArticleCell death & disease2020
Sphingosine kinase 1 regulates HMGB1 translocation by directly interacting with calcium/calmodulin protein kinase II-δ in sepsis-associated liver injury.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Fisetin Attenuates Uterine Leiomyoma in Rats: Potential Crosstalk Between HMGB1, SphK1/S1P, and TGF-β Signaling.Journal of biochemical and molecular toxicology · 2026Article
- Human Breast Milk-Derived Exosomal FP671120.4 Inhibits Macrophage M1 Polarization via Modulating the ELAVL1/Nrf2 Axis in Sepsis-Associated Liver Injury.The Kaohsiung journal of medical sciences · 2026Article
- Molecular mechanisms and functions of protein acetylation in sepsis and sepsis-associated organ dysfunction.Cellular & molecular biology letters · 2025Review
- Bromodomain protein 4 inhibitor JQ-1 alleviates hepatic ischemia-reperfusion injury by blocking the NLRP3/caspase-1 pathway.World journal of emergency medicine · 2025Article
- Bioinformatics study of the TNFRSF1A mechanism involved in acute liver injury in sepsis through the mTOR signaling pathway.Histology and histopathology · 2025Article
- Single-cell transcriptional profiling revealed the protective effects of Buddleoside in sepsis-associated acute liver injury.Frontiers in immunology · 2025Article
- Emerging Roles of High-mobility Group Box-1 in Liver Disease.Journal of clinical and translational hepatology · 2024Review
- Sphk1 regulates HMGB1 via HDAC4 and mediates epithelial pyroptosis in allergic rhinitis.The World Allergy Organization journal · 2024Article
- Musashi-2 potentiates colorectal cancer immune infiltration by regulating the post-translational modifications of HMGB1 to promote DCs maturation and migration.Cell communication and signaling : CCS · 2024Article
- The Impact of Sphingosine Kinases on Inflammation-Induced Cytokine Release and Vascular Endothelial Barrier Integrity.International journal of molecular sciences · 2022Article
- NCell death discovery · 2022Article
- The mechanism of HMGB1 secretion and release.Experimental & molecular medicine · 2022Review
- Review: The role of HMGB1 in spinal cord injury.Frontiers in immunology · 2022Review
- SP1 Promotes HDAC4 Expression and Inhibits HMGB1 Expression to Reduce Intestinal Barrier Dysfunction, Oxidative Stress, and Inflammatory Response after Sepsis.Journal of innate immunity · 2022Article
- Signaling pathways and intervention therapies in sepsis.Signal transduction and targeted therapy · 2021Review
- Prophylactic effect of myricetin and apigenin against lipopolysaccharide-induced acute liver injury.Molecular biology reports · 2021Article
- Therapeutic Efficacy of Excretory-Secretory Products ofFrontiers in cellular and infection microbiology · 2021Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previously, we confirmed that sphingosine kinase 1 (SphK1) inhibition improves sepsis-associated liver injury. High-mobility group box 1 (HMGB1) translocation participates in the development of acute liver failure. However, little information is available on the association between SphK1 and HMGB1 translocation during sepsis-associated liver injury. In the present study, we aimed to explore the effect of SphK1 inhibition on HMGB1 translocation and the underlying mechanism during sepsis-associated liver injury. Primary Kupffer cells and hepatocytes were isolated from SD rats. The rat model of sepsis-associated liver damage was induced by intraperitoneal injection with lipopolysaccharide (LPS). We confirmed that Kupffer cells were the cells primarily secreting HMGB1 in the liver after LPS stimulation. LPS-mediated HMGB1 expression, intracellular translocation, and acetylation were dramatically decreased by SphK1 inhibition. Nuclear histone deacetyltransferase 4 (HDAC4) translocation and E1A-associated protein p300 (p300) expression regulating the acetylation of HMGB1 were also suppressed by SphK1 inhibition. HDAC4 intracellular translocation has been reported to be controlled by the phosphorylation of HDAC4. The phosphorylation of HDAC4 is modulated by CaMKII-δ. However, these changes were completely blocked by SphK1 inhibition. Additionally, by performing coimmunoprecipitation and pull-down assays, we revealed that SphK1 can directly interact with CaMKII-δ. The colocalization of SphK1 and CaMKII-δ was verified in human liver tissues with sepsis-associated liver injury. In conclusion, SphK1 inhibition diminishes HMGB1 intracellular translocation in sepsis-associated liver injury. The mechanism is associated with the direct interaction of SphK1 and CaMKII-δ.
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