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Details for anatomical structure: lipocyte of liver

EndoNet ID: ENC00424

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Synonyms

lipocyte of liver, fat-storing cell, Lipocytus perisinisoideus

General information

The fat-storing cell are involved in the accumulation of fat and vitamin A, as well as the production of intralobular collagen and reticular fibers; under certain pathological conditions, they may be transformed into adipose cells or fibroblasts

Links to other resources

Cytomer cy0011236

Larger structures

    Substructures

      Secreted hormones

      • Hormone: IL-10

      • Hormone: IGFBP-3

        • IGF-I induced IGFBP-3 and IGFBP-5 proteins in a time-dependent manner without an increase in the corresponding mRNAs. [1]
      • Hormone: IGFBP-5

        • IGF-I induced IGFBP-3 and IGFBP-5 proteins in a time-dependent manner without an increase in the corresponding mRNAs. [1]
      • Hormone: IGFBP-2

        • HSCs express IGFBP-2 through IGFBP-6 mRNAs. [1]
      • Hormone: IGFBP-4

        • IGFBP-4 protein levels decreased in response to IGF-I. [1]
      • Hormone: IGFBP-6

      • Hormone: CTGF

        • Human and experimental liver fibrosis is associated with CTGF expression through up-regulation of CTGF mRNA by hepatic stellate cells. [2]
        • CTGF is a fibrogenic cytokine stimulated by TGF-beta1 and may mediate some of TGF-beta1's fibrogenic activity. [3]
      • Hormone: PGE2

      • Hormone: C-C motif chemokine 2

        • Activin A was also found to stimulate CCL2 expression and to activate ERK, JNK, p38, and their downstream targets. [4]
        • HSCs coordinate the liver wound-healing response through secretion of several cytokines and chemokines, including CCL2 (formerly known as monocyte chemoattractant protein-1). [4]
        • SB203580 and SP600125 dose-dependently inhibited CCL2 secretion and gene expression induced by IL-1 or TNF. [4]
      • Hormone: IL-8

        • The induction of CXCL8 (IL-8) expression by IL-1 was inhibited by SP600125. [4]
      • Hormone: TGF-beta 1

        Influenced by:

        • angiotensin II type 1 receptor
          in lipocyte_of_liver
          • Angiotensin II receptor antagonist may also suppress the HSC activation through the decrease of TGF-beta1. [5]
      • Hormone: fibronectin

      • Hormone: RANTES

        • Human hepatic stellate cells express CCR5 and RANTES to induce proliferation and migration. [6]
        • RANTES is elevated in patients with alcoholic hepatitis or chronic hepatitis C. [6]

        Influenced by:

        • CD40
          in lipocyte_of_liver
          • RANTES mRNA and protein secretion were strongly induced after stimulating HSCs with TNF-alpha, IL-1beta, or CD40L. [6]
        • TNFR1
          in lipocyte_of_liver
          • Hepatic stellate cells secrete RANTES after stimulation with TNF-alpha, IL-1beta, and CD40L in an inhibitor-kappaB (I kappa B)kinase (IKK)2/NF kappaB- and JNK-dependent manner. [6]
        • TNFR2
          in lipocyte_of_liver
          • Hepatic stellate cells secrete RANTES after stimulation with TNF-alpha, IL-1beta, and CD40L in an inhibitor-kappaB (I kappa B)kinase (IKK)2/NF kappaB- and JNK-dependent manner. [6]
        • IL-1RI
          in lipocyte_of_liver
          • Hepatic stellate cells secrete RANTES after stimulation with TNF-alpha, IL-1beta, and CD40L in an inhibitor-kappaB (I kappa B)kinase (IKK)2/NF kappaB- and JNK-dependent manner. [6]
        • IL-1RII
          in lipocyte_of_liver
          • Hepatic stellate cells secrete RANTES after stimulation with TNF-alpha, IL-1beta, and CD40L in an inhibitor-kappaB (I kappa B)kinase (IKK)2/NF kappaB- and JNK-dependent manner. [6]
        • CCR5
          in lipocyte_of_liver
          • Hepatic stellate cell derived RANTES acts on hepatic stellate cells in an autocrine fashion. [6]
          • Activated hepatic stellate cells express CCR5 and respond to recombinant human (rh)RANTES stimulation with an increase in proliferation and migration in a CCR5-dependent manner. [6]
          • Even under inflammatory conditions, RANTES would exert biological effects in a paracrine rather than an autocrine fashion. [6]
      • Hormone: GRObeta

        • HSCs produce a variety of chemokines including macrophage inflammatory protein-2 (MIP-2, GRObeta). [6]
      • Hormone: fas Ligand

        • CD95 (APO-1/Fas) and CD95L (APO-1-/Fas-ligand) became increasingly expressed during the course of HSC activation. [7]
      • Hormone: angiotensin II

        • HSCs incubated in the absence of angiotensinogen secreted moderate amounts of ANGII to the culture media. In contrast, incubation with angiotensinogen resulted in a dramatic increase in ANGII secretion. [8]

        Influenced by:

        • angiotensin II type 1 receptor
          in lipocyte_of_liver
      • Hormone: angiotensinogen

      • Hormone: renin

      Receptors

      • Receptor: TLR2

        • HSCs express TLR2, a receptor for Gram-positive bacterial cell wall components, such as peptidoglycan and lipoteichoic acid. [9]

        Induced phenotype:

        • regulation of innate immune response
          • Upregulated TLR2 expression primes HSCs to increase NF-kappa B activation and IL-8 production in response to TLR2 ligands. This is important for the induction of potent innate immune response. [10]
          • HSCs barely respond to TLR2 ligands. Initiation by inflammatory mediators such as TNF-α, IL-1β, and LPS might be required for fulfilling TLR2 signaling in HSCs. [11]
      • Receptor: LRP5

        Induced phenotype:

        • positive regulation of cell-matrix adhesion
          • Cultured rat hepatic stellate cells (HSCs) produce CTGF which is a cell adhesion factor for activated HSCs. LRP is a receptor for CTGF. [12]
          • LRP is utilized by HSCs for binding to CTGF and so this cell surface molecule may be involved in mediating CTGF activity or adhesive signaling during the activation process. [12]
      • Receptor: TLR4

        • Activated human HSCs express TLR4 and its coreceptors MD-2 and CD14. [13]

        Induced phenotype:

        • regulation of innate immune response
          • TLR4-stimulated HSCs produce various chemokines and express adhesion molecules to recruit Kupffer cells and/or circulating macrophages by the site of HSCs. [14]
          • The activation of TLR4 signaling enhances TGF-β signaling, that downregulates the expression of BMP and activin membrane bound inhibitor (Bambi) for firogenic response. [11]
      • Receptor: CD14

        • Activated human HSCs express TLR4 and its coreceptors MD-2 and CD14. [13]

        Induced phenotype:

        • regulation of innate immune response
          • Activated human HSCs express TLR4 and its coreceptor CD14.TLR4 signaling in HSCs enhances the recruitment of inflammatory cells and downregulates BMP and activin membrane bound inhibitor (Bambi) for fibrogenic response. [11]
      • Receptor: CD40

        Influences:

        • RANTES
          • RANTES mRNA and protein secretion were strongly induced after stimulating HSCs with TNF-alpha, IL-1beta, or CD40L. [6]
      • Receptor: CCR5

        Induced phenotype:

        • hepatic stellate cell migration
          • RANTES potently stimulates the migration of hepatic stellate cells due to binding to CCR5, and induces FAK phosphorylation. [6]
        • ERK activation
          • RANTES induces the activation of ERK this biological effect is mediated by CCR5. [6]
        • positive regulation of cell proliferation
          • RANTES stimulates [3H]thymidine incorporation and hepatic stellate cell proliferation in a redox- and intracellular calium-dependent manner, this biological effect is mediated by CCR5. [6]

        Influences:

        • RANTES
          • Hepatic stellate cell derived RANTES acts on hepatic stellate cells in an autocrine fashion. [6]
          • Activated hepatic stellate cells express CCR5 and respond to recombinant human (rh)RANTES stimulation with an increase in proliferation and migration in a CCR5-dependent manner. [6]
          • Even under inflammatory conditions, RANTES would exert biological effects in a paracrine rather than an autocrine fashion. [6]
      • Receptor: fas receptor

        Induced phenotype:

        • negative regulation of apoptosis
          • CD95 ligand and other death receptor ligands act as mitogens in quiescent HSCs with simultaneous inhibition of proapoptotic signaling through an inactivating tyrosine nitration of the CD95 death receptor. [15]
      • Receptor: LXR-alpha

        Induced phenotype:

        • positive regulation of fatty acid biosynthetic process
          • LXR as a master lipogenic transcription factor, as it directly regulates both sterol regulatory element-binding protein 1c (SREBP-1c) and carbohydrate response element-binding protein (ChREBP) to enhance hepatic fatty acid synthesis. [16]
      • Receptor: PPARgamma1

        Induced phenotype:

        • involvement in liver steatosis
          • Among genes involved in lipid metabolism, adipogenesis-related genes, PPARgamma and its targeted gene, CD36 mRNA expression is specifically up-regulated in the liver by high fat diet for 2 weeks. Protein expression of cAMP response element-binding protein (CREB), an upstream molecule of PPARgamma, in the liver was drastically suppressed by high fat diet. [17]
          • CREB-PPARgamma signaling pathway could be involved in the high fat diet-induced liver steatosis. [17]
      • Receptor: angiotensin II type 1 receptor

        Influences:

        • TGF-beta 1
          • Angiotensin II receptor antagonist may also suppress the HSC activation through the decrease of TGF-beta1. [5]
        • angiotensin II
      • Receptor: angiotensin receptor 2

        Induced phenotype:

        • regulation of tissue remodeling
          • The renin-angiotensin system plays an important role in hepatic fibrogenesis. After activation, human hepatic stellate cells express the components of the renin-angiotensin system and synthesize angiotensin II,which lead to the suggestions that locally generated angiotensin II could participate in tissue remodeling in the human liver. [8]
      • Receptor: ETA-R

        Induced phenotype:

        • actin-mediated cell contraction
          • Interactions between endothelin-1 and hepatic stellate cells induces contractility of stellate cells from normal and cirrhotic rat liver. [18]
          • Endothelin-A and endothelin-B receptor antagonist reduces portal pressure in portal hypertensive animals, consistent with its inhibitory effect on stellate cell contraction. [18]
          • Stellate cell contractility increases with progressive liver injury and is proportional to the degree of stellate cell activation, becoming most prominent in the cirrhotic liver. Endothelin-stimulated contraction of stellate cells in cirrhotic liver may contribute to increased intrahepatic resistance and portal pressure. [18]
      • Receptor: ETB-R

        Induced phenotype:

        • actin-mediated cell contraction
          • Interactions between endothelin-1 and hepatic stellate cells induces contractility of stellate cells from normal and cirrhotic rat liver. [18]
          • Endothelin-A and endothelin-B receptor antagonist reduces portal pressure in portal hypertensive animals, consistent with its inhibitory effect on stellate cell contraction. [18]
          • Stellate cell contractility increases with progressive liver injury and is proportional to the degree of stellate cell activation, becoming most prominent in the cirrhotic liver. Endothelin-stimulated contraction of stellate cells in cirrhotic liver may contribute to increased intrahepatic resistance and portal pressure. [18]
      • Receptor: PDGFR

        • PDGFs form a family of dimeric isoforms inducing growth stimulation, chemotaxis, cell shape changes, and intracellular signaling in HSC from mouse, rat, or humans. [19]

        Induced phenotype:

        • regulation of tissue remodeling
          • Dominant-negative soluble PDGF-beta receptor is active as an antifibrogenic protein drug able to reduce the biological effects of PDGF in ongoing fibrogenesis. Therefore, it could be an attractive therapeutic agent for the treatment of fibrotic liver diseases and possibly other fibrotic organ lesions. [19]
          • PDGF plays a critical role in the progression and initiation of experimental liver fibrogenesis, it is important for the activation into a myofibroblastic phenotype. [20]
      • Receptor: EGFR isoform a

        Induced phenotype:

        • positive regulation of cell proliferation and apotosis
          • In quiescent HSC, hydrophobic bile acids activate the EGFR, and this can couple to both cell proliferation and apoptosis, depending on the JNK signaling. Therefore, JNK act as a switch between bile acid-induced proliferation and apoptosis in HSC. [21]
      • Receptor: PDGFRbeta

        • PDGF receptor type b (PDGFRb) is acquired as the cells undergo myofibroblastic phenotypic changes. [22]

        Induced phenotype:

        • regulation of tissue remodeling
          • Dominant-negative soluble PDGF-beta receptor is active as an antifibrogenic protein drug able to reduce the biological effects of PDGF in ongoing fibrogenesis. Therefore, it could be an attractive therapeutic agent for the treatment of fibrotic liver diseases and possibly other fibrotic organ lesions. [19]
          • PDGF plays a critical role in the progression and initiation of experimental liver fibrogenesis, it is important for the activation into a myofibroblastic phenotype. [20]
      • Receptor: TNFR2

        Influences:

        • RANTES
          • Hepatic stellate cells secrete RANTES after stimulation with TNF-alpha, IL-1beta, and CD40L in an inhibitor-kappaB (I kappa B)kinase (IKK)2/NF kappaB- and JNK-dependent manner. [6]
      • Receptor: TNFR1

        Influences:

        • RANTES
          • Hepatic stellate cells secrete RANTES after stimulation with TNF-alpha, IL-1beta, and CD40L in an inhibitor-kappaB (I kappa B)kinase (IKK)2/NF kappaB- and JNK-dependent manner. [6]
      • Receptor: IL-1RI

        Influences:

        • RANTES
          • Hepatic stellate cells secrete RANTES after stimulation with TNF-alpha, IL-1beta, and CD40L in an inhibitor-kappaB (I kappa B)kinase (IKK)2/NF kappaB- and JNK-dependent manner. [6]
      • Receptor: IL-1RII

        Influences:

        • RANTES
          • Hepatic stellate cells secrete RANTES after stimulation with TNF-alpha, IL-1beta, and CD40L in an inhibitor-kappaB (I kappa B)kinase (IKK)2/NF kappaB- and JNK-dependent manner. [6]
      • Receptor: TGF-beta type I receptor

      Reference