scholarly journals Differential Effects of Endotoxin Lipopolysaccharide on Stellate Cells and Portal Fibroblasts: Implications in Fibrosis Originating in Central Versus Portal Injury

2021 ◽  
Vol 35 (S1) ◽  
Author(s):  
Akanksha Sharma ◽  
Chandrashekhar Gandhi
Keyword(s):  
Stellate Cells ◽  
Differential Effects ◽  
Portal Fibroblasts

Secretion of MCP-1/CCL2 by bile duct epithelia induces myofibroblastic transdifferentiation of portal fibroblasts

2006 ◽  
Vol 290 (4) ◽  
pp. G765-G771 ◽  
Author(s):  
Emma A. Kruglov ◽  
Rebecca A. Nathanson ◽  
Trong Nguyen ◽  
Jonathan A. Dranoff
Keyword(s):  
Bile Duct ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Functional Responses ◽  
Blocking Antibody ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Portal Fibroblasts ◽  
Expression Loss

Portal fibroblasts (PF) are fibrogenic liver cells distinct from hepatic stellate cells (HSC). Recent evidence suggests that PF may be important mediators of biliary fibrosis and cirrhosis. The cytokine monocyte chemoattractant protein-1 (MCP-1)/CCL2 is upregulated in biliary fibrosis by bile duct epithelia (BDE) and induces functional responses in HSC. Thus we hypothesized that release of MCP-1 may mediate biliary fibrosis. We report that PF express functional receptors for MCP-1 that are distinct from the receptor CCR2. MCP-1 induces proliferation, increase and redistribution of α-smooth muscle (α-SMA) expression, loss of the ectonucleotidase NTPDase2, and upregulation of α1-procollagen production in PF. BDE secretions induce α-SMA levels in PF, and this is inhibited by MCP-1 blocking antibody. Together, these data suggest that BDE regulate PF proliferation and myofibroblastic transdifferentiation in a paracrine fashion via release of MCP-1.

scholarly journals Characterization of hepatic stellate cells, portal fibroblasts, and mesothelial cells in normal and fibrotic livers

2016 ◽  
Vol 64 (5) ◽  
pp. 1137-1146 ◽  
Author(s):  
Ingrid Lua ◽  
Yuchang Li ◽  
Jessica A. Zagory ◽  
Kasper S. Wang ◽  
Samuel W. French ◽  
...  
Keyword(s):  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Mesothelial Cells ◽  
Portal Fibroblasts

scholarly journals The role of Mesothelin signaling in Portal Fibroblasts in the pathogenesis of cholestatic liver fibrosis

2021 ◽  
Vol 8 ◽  
Author(s):  
Hiroaki Fuji ◽  
Grant Miller ◽  
Takahiro Nishio ◽  
Yukinori Koyama ◽  
Kevin Lam ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Liver Injury ◽  
Hepatic Stellate Cells ◽  
Inflammatory Responses ◽  
Stellate Cells ◽  
Collagen Type I ◽  
Type I ◽  
Fibrotic Liver ◽  
Portal Fibroblasts

Liver fibrosis develops in response to chronic toxic or cholestatic injury, and is characterized by apoptosis of damaged hepatocytes, development of inflammatory responses, and activation of Collagen Type I producing myofibroblasts that make liver fibrotic. Two major cell types, Hepatic Stellate Cells (HSCs) and Portal Fibroblasts (PFs) are the major source of hepatic myofibroblasts. Hepatotoxic liver injury activates Hepatic Stellate Cells (aHSCs) to become myofibroblasts, while cholestatic liver injury activates both aHSCs and Portal Fibroblasts (aPFs). aPFs comprise the major population of myofibroblasts at the onset of cholestatic injury, while aHSCs are increasingly activated with fibrosis progression. Here we summarize our current understanding of the role of aPFs in the pathogenesis of cholestatic fibrosis, their unique features, and outline the potential mechanism of targeting aPFs in fibrotic liver.

Activated hepatic stellate cells and portal fibroblasts contribute to cholestatic liver fibrosis in MDR2 knockout mice

2019 ◽  
Vol 71 (3) ◽  
pp. 573-585 ◽  
Author(s):  
Takahiro Nishio ◽  
Ronglin Hu ◽  
Yukinori Koyama ◽  
Shuang Liang ◽  
Sara B. Rosenthal ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Knockout Mice ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Activated Hepatic Stellate Cells ◽  
Portal Fibroblasts

p75 Neurotrophin Receptor Is a Marker for Precursors of Stellate Cells and Portal Fibroblasts in Mouse Fetal Liver

2008 ◽  
Vol 135 (1) ◽  
pp. 270-281.e3 ◽  
Author(s):  
Kaori Suzuki ◽  
Minoru Tanaka ◽  
Natsumi Watanabe ◽  
Shigeru Saito ◽  
Hidenori Nonaka ◽  
...  
Keyword(s):  
Fetal Liver ◽  
Stellate Cells ◽  
Neurotrophin Receptor ◽  
P75 Neurotrophin Receptor ◽  
Portal Fibroblasts

scholarly journals Endoglin Trafficking/Exosomal Targeting in Liver Cells Depends on N-Glycosylation

Cells ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 997 ◽  
Author(s):  
Meurer ◽  
Wimmer ◽  
Leur ◽  
Weiskirchen
Keyword(s):  
Bone Morphogenetic Proteins ◽  
Hepatic Stellate Cells ◽  
Transforming Growth Factor ◽  
Stellate Cells ◽  
Transforming Growth Factor Β ◽  
Liver Cells ◽  
Type I ◽  
Caveolin 1 ◽  
Portal Fibroblasts ◽  
Opposing Effects

Injury of the liver involves a wound healing partial reaction governed by hepatic stellate cells and portal fibroblasts. Individual members of the transforming growth factor-β (TGF-β) superfamily including TGF-β itself and bone morphogenetic proteins (BMP) exert diverse and partially opposing effects on pro-fibrogenic responses. Signaling by these ligands is mediated through binding to membrane integral receptors type I/type II. Binding and the outcome of signaling is critically modulated by Endoglin (Eng), a type III co-receptor. In order to learn more about trafficking of Eng in liver cells, we investigated the membranal subdomain localization of full-length (FL)-Eng. We could show that FL-Eng is enriched in Caveolin-1-containing sucrose gradient fractions. Since lipid rafts contribute to the pool of exosomes, we could consequently demonstrate for the first time that exosomes isolated from cultured primary hepatic stellate cells and its derivatives contain Eng. Moreover, via adenoviral overexpression, we demonstrate that all liver cells have the capacity to direct Eng to exosomes, irrespectively whether they express endogenous Eng or not. Finally, we demonstrate that block of N-glycosylation does not interfere with dimerization of the receptor, but abrogates the secretion of soluble Eng (sol-Eng) and prevents exosomal targeting of FL-Eng.

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