scholarly journals The Hepatic Sinusoid in Aging and Disease: Update and Advances From the 20th Liver Sinusoid Meeting

2020 ◽  
Vol 4 (7) ◽  
pp. 1087-1098
Author(s):  
Martí Ortega‐Ribera ◽  
Nicholas J. Hunt ◽  
Jordi Gracia‐Sancho ◽  
Victoria C. Cogger
Keyword(s):  
Liver Sinusoid ◽  
Hepatic Sinusoid

scholarly journals Monocyte-induced recovery of inflammation-associated hepatocellular dysfunction in a biochip-based human liver model

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Marko Gröger ◽  
Knut Rennert ◽  
Benjamin Giszas ◽  
Elisabeth Weiß ◽  
Julia Dinger ◽  
...  
Keyword(s):  
Liver Dysfunction ◽  
Human Liver ◽  
Immune Cell ◽  
Early Event ◽  
Liver Sinusoid ◽  
Human Sepsis ◽  
Cellular Events ◽  
Cell Layers ◽  
Parenchymal Cells

Abstract Liver dysfunction is an early event in sepsis-related multi-organ failure. We here report the establishment and characterization of a microfluidically supported in vitro organoid model of the human liver sinusoid. The liver organoid is composed of vascular and hepatocyte cell layers integrating non-parenchymal cells closely reflecting tissue architecture and enables physiological cross-communication in a bio-inspired fashion. Inflammation-associated liver dysfunction was mimicked by stimulation with various agonists of toll-like receptors. TLR-stimulation induced the release of pro- and anti-inflammatory cytokines and diminished expression of endothelial VE-cadherin, hepatic MRP-2 transporter and apolipoprotein B (ApoB), resulting in an inflammation-related endothelial barrier disruption and hepatocellular dysfunction in the liver organoid. However, interaction of the liver organoid with human monocytes attenuated inflammation-related cell responses and restored MRP-2 transporter activity, ApoB expression and albumin/urea production. The cellular events observed in the liver organoid closely resembled pathophysiological responses in the well-established sepsis model of peritoneal contamination and infection (PCI) in mice and clinical observations in human sepsis. We therefore conclude that this human liver organoid model is a valuable tool to investigate sepsis-related liver dysfunction and subsequent immune cell-related tissue repair/remodeling processes.

scholarly journals Surface charge distribution on the endothelial cell of liver sinusoids.

1984 ◽  
Vol 99 (2) ◽  
pp. 639-647 ◽  
Author(s):  
L Ghitescu ◽  
A Fixman
Keyword(s):  
Endothelial Cell ◽  
Cell Surface ◽  
Liver Sinusoid ◽  
Electron Microscopic ◽  
Coated Pits ◽  
Endothelial Cell Surface ◽  
Liver Sinusoids ◽  
Surface Charge Distribution ◽  
Cationic Residues

The topography of the charged residues on the endothelial cell surface of liver sinusoid capillaries was investigated by using electron microscopic tracers of different size and charge. The tracers used were native ferritin (pl 4.2-4.7) and its cationized (pl 8.4) and anionized (pl 3.7) derivatives, BSA coupled to colloidal gold (pl of the complex 5.1), hemeundecapeptide (pl 4.85), and alcian blue (pl greater than 10). The tracers were either injected in vivo or perfused in situ through the portal vein of the mouse liver. In some experiments, two tracers of opposite charge were sequentially perfused with extensive washing in between. The liver was processed for electron microscopy and the binding pattern of the injected markers was recorded. The electrostatic nature of the tracer binding was assessed by perfusion with high ionic strength solutions, by aldehyde quenching of the plasma membrane basic residues, and by substituting the cell surface acidic moieties with positively charged groups. Results indicate that the endothelial cells of the liver sinusoids expose on their surface both cationic and anionic residues. The density distribution of these charged groups on the cell surface is different. While the negative charge is randomly and patchily scattered all over the membrane, the cationic residues seem to be accumulated in coated pits. The charged groups co-exist in the same coated pit and bind the opposite charged macromolecule. It appears that the fixed positive and negative charges of the coated pit glycocalyx are mainly segregated in space. The layer of basic residues is located at 20-30-nm distance of the membrane, while most of the negative charges lie close to the external leaflet of the plasmalemma.

Influence of microflow on hepatic sinusoid blood flow and red blood cell deformation

2021 ◽  
Author(s):  
Tianhao Wang ◽  
Shouqin Lü ◽  
Yinjing Hao ◽  
Zinan Su ◽  
Mian Long ◽  
...  
Keyword(s):  
Blood Flow ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Cell Deformation ◽  
Hepatic Sinusoid

Dose- and Time-Dependent Effects of Ethanol on Functional and Structural Aspects of the Liver Sinusoid in the Mouse

1997 ◽  
Vol 21 (6) ◽  
pp. 1128-1136 ◽  
Author(s):  
G. Sarphie ◽  
N. B. D'Souza ◽  
D. H. Thiel ◽  
D. Hill ◽  
C. J. McClain ◽  
...  
Keyword(s):  
Time Dependent ◽  
Liver Sinusoid ◽  
Structural Aspects

Mechanism for phosphatidylserine-dependent erythrophagocytosis in mouse liver

Blood ◽  
2011 ◽  
Vol 117 (19) ◽  
pp. 5215-5223 ◽  
Author(s):  
Sung-Jin Lee ◽  
Seung-Yoon Park ◽  
Mi-Yeon Jung ◽  
Sang Mun Bae ◽  
In-San Kim
Keyword(s):  
Kupffer Cells ◽  
Mouse Liver ◽  
Blood Circulation ◽  
Dependent Manner ◽  
Potential Mechanism ◽  
Phagocytic Capacity ◽  
Hepatic Sinusoid ◽  
In Vivo Animal Model ◽  
Hepatic Sinusoidal Endothelial Cells

Abstract Aged or damaged RBCs are effectively removed from the blood circulation by Kupffer cells in the liver, but little is known regarding the mechanism of the clearance process. Here we show that stabilin-1 and stabilin-2 in hepatic sinusoidal endothelial cells (HSECs) are critical in effectively clearing damaged RBCs in mouse liver. Damaged RBCs and phosphatidylserine (PS)–coated beads were effectively sequestered in the hepatic sinusoid regardless of the presence of Kupffer cells, suggesting a role for HSECs in PS-dependent sequestration of PS-exposed RBCs in the liver. HSECs mediate tethering of damaged RBCs in a PS-dependent manner via stabilin-1 and stabilin-2. In a sinusoid-mimicked coculture system consisting of macrophages layered over HSECs, there was significant enhancement of the phagocytic capacity of macrophages, and this was mediated by stabilin-1 and stabilin-2 in HSECs. Liver-specific knockdown of stabilin-1 and stabilin-2 inhibited the sequestration of damaged RBCs in the hepatic sinusoid and delayed the elimination of damaged cells in an in vivo animal model. Thus, the roles of stabilin-1 and stabilin-2 in hepatic sequestration of PS-exposed RBCs may represent a potential mechanism for the clearance of damaged RBCs by Kupffer cells and for the control of some pathologic conditions such as hemolytic anemia.

scholarly journals 15th International Symposium on Cells of the Hepatic Sinusoid, 2010

2011 ◽  
Vol 31 (6) ◽  
pp. 762-772 ◽  
Author(s):  
Laurie D. DeLeve ◽  
Hartmut Jaeschke ◽  
Vijay K. Kalra ◽  
Kinji Asahina ◽  
David A. Brenner ◽  
...  
Keyword(s):  
International Symposium ◽  
Hepatic Sinusoid ◽  
15Th International Symposium

scholarly journals Transcriptional Dynamics of Hepatic Sinusoid‐Associated Cells After Liver Injury

Hepatology ◽  
2020 ◽  
Vol 72 (6) ◽  
pp. 2119-2133 ◽  
Author(s):  
Mike K. Terkelsen ◽  
Sofie M. Bendixen ◽  
Daniel Hansen ◽  
Emma A.H. Scott ◽  
Andreas F. Moeller ◽  
...  
Keyword(s):  
Liver Injury ◽  
Hepatic Sinusoid ◽  
Transcriptional Dynamics
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