ArticleJournal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract2007
Protein kinase C-zeta (PKC-zeta) regulates Kupffer cell apoptosis during experimental sepsis.
Article in Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 24 citations in OpenAlex.
- Platelet Glycoprotein Ibα Cytoplasmic Tail Exacerbates Thrombosis During Bacterial Sepsis.International journal of molecular sciences · 2024Article
- Dietary mannan oligosaccharides strengthens intestinal immune barrier functionFrontiers in immunology · 2022Article
- lncRNA IL-17RA-1 Attenuates LPS-Induced Sepsis via miR-7847-3p/PRKCG-Mediated MAPK Signaling Pathway.Mediators of inflammation · 2022Article
- PED/PEA-15 inhibits hydrogen peroxide-induced apoptosis in Ins-1E pancreatic beta-cells via PLD-1.PloS one · 2014Article
- Does LKB1 mediate activation of hepatic AMP-protein kinase (AMPK) and sirtuin1 (SIRT1) after Roux-en-Y gastric bypass in obese rats?Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2010Article
- Downregulation of adiponectin/AdipoR2 is associated with steatohepatitis in obese mice.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2009Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundKupffer cells play an important role in sepsis-mediated liver injury. We tested the hypothesis that PKC-zeta plays a critical role in Kupffer cell apoptosis during sepsis.
methodsSepsis was induced in rats by cecal ligation and puncture (CLP); 12 h later, livers were assayed for PKC-zeta, IKKalpha, IKKbeta, IKKgamma, NF-kappaB, Fas/FasL, Caspase-3, and DNA fragmentation. Kupffer cells from control rats were infected with AdPKC-zeta DN to inhibit PKC-zeta, or transfected with pCMVPKC-zeta to overexpress PKC-zeta, and then treated with lipopolysaccharide (LPS). Cellular extracts were assayed for PKC-zeta, IKKalpha, IKKbeta, IKKgamma, NF-kappaB, Fas/FasL, Caspase-3, and DNA fragmentation.
resultsDuring sepsis, PKC-zeta localized in cells positive for the macrophage marker (F4/80). CLP upregulated PKC-zeta protein and activity, IKKbeta, IKKgamma, NF-kappaB, Fas/FasL, Caspase-3, and increased DNA fragmentation in rat livers (all p<0.001). AdPKC-zeta DN attenuated the LPS-induced upregulation of PKC-zeta activity, IKKbeta, IKKgamma, NF-kappaB, Fas/FasL, Caspase-3, and DNA fragmentation in Kupffer cells (all p<0.001), whereas overexpression of PKC-zeta augmented LPS-induced upregulation of IKKbeta, IKKgamma, NF-kappaB, Caspase-3, and DNA fragmentation (p<0.001).
conclusionPKC-zeta plays an important role in sepsis-induced apoptosis of Kupffer cells via activation of NF-kappaB and Fas/FasL. Manipulating the response of Kupffer cells to cellular stress may have important therapeutic implications.
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