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Details for anatomical structure: Kupffer cell stellate cell of liver

EndoNet ID: ENC00273

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Synonyms

Kupffer cell stellate cell of liver, , Macrophagocytus stellatus

General information

phagocytic cell in liver

Links to other resources

Cytomer cy0011374

Larger structures

    Substructures

      Secreted hormones

      • Hormone: IL-1 alpha

        • Kupffer cells lining the hepatic sinusoids are the largest population of resident tissue macrophages of the body, and they are considered to be the main source of inflammatory cytokines. [1]
      • Hormone: IL-1 beta

      • Hormone: TNF-alpha

        • The cytokines of the acute phase reaction are synthesized in the Kupffer cells in the hepatic sinusoids. [1]
        • TNF-alpha is thought to regulate Kupffer cell activation through both autocrine and paracrine mechanisms. [2]

        Influenced by:

        • TLR4
          in Kupffer_cell_stellate_cell_of_liver
          • LPS activates Kupffer cells to produce mediators such as TNF-alpha. [3]
      • Hormone: IL-11

        • Hepatocytes did not express IL-11. [4]
      • Hormone: PDGFA

      • Hormone: RANTES

        • Human hepatic stellate cells express CCR5 and RANTES to induce proliferation and migration. [5]
      • Hormone: TGF-beta 1

      • Hormone: PGE2

      • Hormone: IL-18

        • IL-18 acts on natural killer cells to increase Fas ligand (FasL) that causes liver injury by induction of Fas-dependent hepatocyte apoptosis. [6]
        • Kupffer cells have the potential to induce liver injury by production of IL- 18. [6]

        Influenced by:

        • TLR4
          in Kupffer_cell_stellate_cell_of_liver
          • LPS induces IL-18 secretion from Kupffer cells in a caspase-1-dependent manner. [6]
      • Hormone: ICAM-1

        • Endotoxin activates Kupffer cells to produce mediators such as ICAM-1, which bind polymorphonuclear neutrophils (PMN). [7]
      • Hormone: PGD2

        • Kupffer cells produce prostaglandins, primarily PGD2 and PGE2, which stimulate production of glucose from endogenous hepatic glycogen by activating phosphorylase A. [7]
      • Hormone: interleukin 6

        • Human Kupffer cells activated with CEA, NCA and the peptide PELPK, express IL-1beta, TNF-alpha and IL-6. [8]
      • Hormone: IFN-alpha

        • In liver parenchyma, IFN-alpha was mainly detected in Kupffer cells, and not in hepatocytes. [9]
      • Hormone: IL-8

        • LPS induces the production of inflammatory chemokines including IL-8 and MCP-1 in activated HSCs. [3]

        Influenced by:

        • TLR4
          in Kupffer_cell_stellate_cell_of_liver
          • LPS directly acts through TLR4 and then activates NF-kappa B and JNK to induce proinflammatory chemokines and adhesion molecules in activated human HSCs. [3]

      Receptors

      • Receptor: ferroportin-1

      • Receptor: LRP5

      • Receptor: CD14

      • Receptor: TLR4

        Influences:

        • IL-8
          • LPS directly acts through TLR4 and then activates NF-kappa B and JNK to induce proinflammatory chemokines and adhesion molecules in activated human HSCs. [3]
        • TNF-alpha
          • LPS activates Kupffer cells to produce mediators such as TNF-alpha. [3]
        • IL-18
          • LPS induces IL-18 secretion from Kupffer cells in a caspase-1-dependent manner. [6]
      • Receptor: TNFR1

      • Receptor: TNFR2

      • Receptor: fas receptor

      • Receptor: PRLR

        Induced phenotype:

        • reduction of cytokine gene expression
          • Haemorrhage markedly increases the level of mRNA for IL-1 beta, IL-6, TGF-beta and TNF-beta in Kupffer cells. In vivo PRL treatment significantly decreases the cytokine gene expression in Kupffer cells following haemorrhage. Thus, PRL may be useful in blunting the systemic inflammatory response associated with cell and organ depression following shock. [10]
        • positive regulation of cytokine biosynthetic process
          • In synergy with IFN-gamma, PRL decreases monoblastic growth and increases cytokine gene expression in Kupffer cells after hemorrhage. [10]
      Reference