ArticleThe American journal of pathology2013
Kupffer cells protect liver sinusoidal endothelial cells from Fas-dependent apoptosis in sepsis by down-regulating gp130.
Article in The American journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 45 citations in OpenAlex.
- Loss of type I interferon signaling in Kupffer cells triggers viral spread and fatal liver damage in a mouse model of Crimean-Congo hemorrhagic fever.PLoS pathogens · 2026Article
- From microtubule remodeling to clinical translation: the multifaceted roles of vasohibin-1 in disease modulation.Frontiers in immunology · 2026Review
- Effect of antibiotics on Kupffer cell immunometabolism relative to intracellular killing ofmBio · 2025Article
- Mechanisms of immune suppression in sepsis/shock: one investigator's/lab group's experience (SLB 2024 legacy award presentation).Journal of leukocyte biology · 2025Article
- Gut Microbiota and Liver Dysfunction in Sepsis: The Role of Inflammatory Mediators and Therapeutic Approaches.International journal of molecular sciences · 2024Review
- Cellular uptake and in vivo distribution of mesenchymal-stem-cell-derived extracellular vesicles are protein corona dependent.Nature nanotechnology · 2024Article
- VISTA nonredundantly regulates proliferation and CD69low γδ T cell accumulation in the intestine in murine sepsis.Journal of leukocyte biology · 2024Article
- Impaired hemoglobin clearance by sinusoidal endothelium promotes vaso-occlusion and liver injury in sickle cell disease.Haematologica · 2024Article
- Single-cell RNA sequencing deciphers the mechanism of sepsis-induced liver injury and the therapeutic effects of artesunate.Acta pharmacologica Sinica · 2023Article
- The gp130/STAT3-endoplasmic reticulum stress axis regulates hepatocyte necroptosis in acute liver injury.Croatian medical journal · 2023Article
- Vascular endotheliitis associated with infections: Its pathogenetic role and therapeutic implication.Biochemical pharmacology · 2022Review
- Gasdermin D inhibition prevents multiple organ dysfunction during sepsis by blocking NET formation.Blood · 2021Article
- An Improved Time- and Labor- Efficient Protocol for Mouse Primary Hepatocyte Isolation.Journal of visualized experiments : JoVE · 2021Article
- The two facets of gp130 signalling in liver tumorigenesis.Seminars in immunopathology · 2021Review
- Cellular Mechanisms of Liver Fibrosis.Frontiers in pharmacology · 2021Review
- The role of liver sinusoidal endothelial cells in cancer liver metastasis.American journal of cancer research · 2021Review
- Biomarkers and Associated Immune Mechanisms for Early Detection and Therapeutic Management of Sepsis.Immune network · 2020Review
- [Research progress of liver sinusoidal endothelial cells in the regulation of liver microenvironment to affect liver fibrosis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2020Review
- Kupffer cells promote T-cell hepatitis by producing CXCL10 and limiting liver sinusoidal endothelial cell permeability.Theranostics · 2020Article
- Cystathionine-Gamma-Lyase-Derived Hydrogen Sulfide-Regulated Substance P Modulates Liver Sieve Fenestrations in Caecal Ligation and Puncture-Induced Sepsis.International journal of molecular sciences · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Endothelial cell (EC) dysfunction is a key feature of multiple organ injury, the primary cause of fatality seen in critically ill patients. Although the development of EC dysfunction in the heart and lung is well studied in sepsis, it remains unclear in the liver. Herein, we report that liver sinusoidal ECs (LSECs; defined as CD146(+)CD45(-)) exhibit increased intercellular adhesion molecule-1 (CD54) and Fas in response to sepsis induced by cecal ligation and puncture (CLP). By using magnetically enriched LSEC (CD146(+)) populations, we show evidence of marked apoptosis, with a twofold decline in viable LSECs in CLP animals compared with sham controls. These changes and increased serum alanine aminotransferase levels were all mitigated in septic Fas(-/-) and Fas ligand(-/-) animals. Although we previously reported increased numbers of Fas ligand expressing CD8(+) T lymphocytes in the septic liver, CD8(+) T-cell deficiency did not reverse the onset of LSEC apoptosis/damage. However, Kupffer cell depletion with clodronate liposomes resulted in greater apoptosis and Fas expression after CLP and a decrease in glycoprotein 130 expression on LSECs, suggesting that STAT3 activation may protect these cells from injury. Our results document a critical role for death receptor-mediated LSEC injury and show the first evidence that Kupffer cells are essential to the viability of LSECs, which appears to be mediated through glycoprotein 130 expression in sepsis.
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