Typing of hepatic nonparenchymal cells using fibulin-2 and cytoglobin/STAP as liver fibrogenesis-related markers

2004 ◽  
Vol 122 (1) ◽  
Author(s):  
Yuko Tateaki ◽  
Tomohiro Ogawa ◽  
Norifumi Kawada ◽  
Toshihiko Kohashi ◽  
Koji Arihiro ◽  
...  
Keyword(s):  
Nonparenchymal Cells ◽  
Liver Fibrogenesis ◽  
Hepatic Nonparenchymal Cells

scholarly journals Ultrastructural Characteristics of Rat Hepatic Oval Cells and Their Intercellular Contacts in the Model of Biliary Fibrosis: New Insights into Experimental Liver Fibrogenesis

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Joanna Maria Lotowska ◽  
Maria Elzbieta Sobaniec-Lotowska ◽  
Dariusz Marek Lebensztejn ◽  
Urszula Daniluk ◽  
Piotr Sobaniec ◽  
...  
Keyword(s):  
Bile Duct ◽  
Cell Contact ◽  
Oval Cells ◽  
Cellular Interactions ◽  
Nonparenchymal Cells ◽  
Transmission Electron ◽  
Duct Ligation ◽  
Liver Fibrogenesis ◽  
Direct Cell ◽  
Hepatic Nonparenchymal Cells

Purpose. Recently, it has been emphasized that hepatic progenitor/oval cells (HPCs) are significantly involved in liver fibrogenesis. We evaluated the multipotential population of HPCs by transmission electron microscope (TEM), including relations with adherent hepatic nonparenchymal cells (NPCs) in rats with biliary fibrosis induced by bile duct ligation (BDL). Methods. The study used 6-week-old Wistar Crl: WI(Han) rats after BDL for 1, 6, and 8 weeks. Results. Current ultrastructural analysis showed considerable proliferation of HPCs in experimental intensive biliary fibrosis. HPCs formed proliferating bile ductules and were scattered in periportal connective tissue. We distinguished 4 main types of HPCs: 0, I, II (bile duct-like cells; most common), and III (hepatocyte-like cells). We observed, very seldom presented in literature, cellular interactions between HPCs and adjacent NPCs, especially commonly found transitional hepatic stellate cells (T-HSCs) and Kupffer cells/macrophages. We showed the phenomenon of penetration of the basement membrane of proliferating bile ductules by cytoplasmic processes sent by T-HSCs and the formation of direct cell-cell contact with ductular epithelial cells related to HPCs. Conclusions. HPC proliferation induced by BDL evidently promotes portal fibrogenesis. Better understanding of the complex cellular interactions between HPCs and adjacent NPCs, especially T-HSCs, may help develop antifibrotic therapies in the future.

scholarly journals PPARα-Dependent Activation of Cell Cycle Control and DNA Repair Genes in Hepatic Nonparenchymal Cells

2010 ◽  
Vol 118 (2) ◽  
pp. 404-410 ◽  
Author(s):  
Aijuan Qu ◽  
Yatrik M. Shah ◽  
Tsutomu Matsubara ◽  
Qian Yang ◽  
Frank J. Gonzalez
Keyword(s):  
Cell Cycle ◽  
Dna Repair ◽  
Cell Cycle Control ◽  
Dna Repair Genes ◽  
Nonparenchymal Cells ◽  
Hepatic Nonparenchymal Cells ◽  
Repair Genes

scholarly journals Murine hepatic accessory cells support the proliferation of Th1 but not Th2 helper T lymphocyte clones.

1989 ◽  
Vol 170 (3) ◽  
pp. 985-990 ◽  
Author(s):  
D B Magilavy ◽  
F W Fitch ◽  
T F Gajewski
Keyword(s):  
T Lymphocytes ◽  
Antibody Responses ◽  
Th2 Cells ◽  
Accessory Cell ◽  
Spleen Cells ◽  
Nonparenchymal Cells ◽  
Accessory Cells ◽  
Splenic Cells ◽  
Hepatic Nonparenchymal Cells ◽  
Th1 And Th2

The liver is the major site of clearance and degradation of foreign antigens from the portal circulation. Despite the presence of hepatic accessory cells, antibody responses to orally administered antigens are uncommon. To ascertain if hepatic accessory cells are incapable of stimulating specific subsets of T lymphocytes, freshly isolated hepatic nonparenchymal and splenic cells were cultured with a panel of antigen-specific, H-2-restricted Th1 and Th2 HTL clones. Whereas spleen cells stimulated the proliferation of both Th1 and Th2 clones, hepatic nonparenchymal cells (NPC) stimulated the proliferation of only Th1 and not Th2 clones. Adding rIL-1, rIL-6, and rIL-7, alone or in combination, to the cultures did not result in proliferation of the Th2 clones. Despite the absence of Th2 proliferation, NPC were able to stimulate the secretion of IL-3 and IL-4 by Th2 clones in the presence of antigen. Moreover, adding hepatic NPC did not inhibit spleen cells from stimulating Th2 clones in the presence of antigen. Thus, the inability of liver cells to stimulate the proliferation of Th2 helper T lymphocytes appears to be secondary to an absence of either an unknown accessory cell cofactor or an accessory cell that preferentially presents antigen to Th2 cells. The selective activation of Th1 and not Th2 cells by liver accessory cells may result in suppression of antibody responses to orally administered antigens.

scholarly journals Cre-ativity in the liver: Transgenic approaches to targeting hepatic nonparenchymal cells

Hepatology ◽  
2015 ◽  
Vol 61 (6) ◽  
pp. 2091-2099 ◽  
Author(s):  
Stephen N. Greenhalgh ◽  
Kylie P. Conroy ◽  
Neil C. Henderson
Keyword(s):  
Nonparenchymal Cells ◽  
Hepatic Nonparenchymal Cells

scholarly journals The Value of Circulating Nogo-B for Evaluating Hepatic Functional Reserve in Patients with Cirrhosis

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Maoyao Wen ◽  
Ruoting Men ◽  
Zongze Yang ◽  
Xuelian Dan ◽  
Wenchao Wu ◽  
...  
Keyword(s):  
Liver Cirrhosis ◽  
Surrogate Marker ◽  
High Plasma ◽  
Enzyme Linked Immunosorbent Assay ◽  
Clinical Parameters ◽  
Healthy Controls ◽  
Nonparenchymal Cells ◽  
Esophagogastric Varices ◽  
Pugh Class ◽  
Hepatic Nonparenchymal Cells

Objective. To examine Nogo-B in liver tissues and plasma of patients with liver cirrhosis and associate them with various clinical parameters.Materials and Methods. Nogo-B protein expression was examined by immunohistochemistry in 24 human fibrotic/cirrhotic liver specimens and 10 healthy controls. We determined plasma Nogo-B levels by enzyme-linked immunosorbent assay in 301 patients with liver cirrhosis and 153 healthy controls, and then analyzed various clinical parameters.Results. Nogo-B was mainly expressed in nonparenchymal cells in the liver and was marked increased in liver with significant fibrosis/cirrhosis compared to controls. Moreover, Metavir F4 showed a higher level of expression than F2. Plasma Nogo-B levels were significantly higher in cirrhotic patients than in healthy controls and were the highest in Child-Pugh class C patients. Plasma Nogo-B levels were positively correlated with Child-Pugh scores. However, there was no relationship between plasma Nogo-B levels and etiology of liver diseases, ALT, AST, platelet counts, and the severity of esophagogastric varices.Conclusions. Nogo-B is mainly expressed in hepatic nonparenchymal cells and is present in plasma. Abnormally high plasma levels of Nogo-B are associated with hepatic cirrhosis and Child-Pugh score, but not correlated with the grade of liver inflammation or portal hypertension. Plasma Nogo-B may be a novel surrogate marker to reflect liver function reserve.

scholarly journals Carbachol Induces Hepatocyte Proliferation, but Only in the Presence of Hepatic Nonparenchymal Cells

2007 ◽  
Vol 57 (3) ◽  
pp. 139-145 ◽  
Author(s):  
Ryoichi Yoshimura ◽  
Shingo Somekawa ◽  
Hiroshi Omori ◽  
Yasuhisa Endo
Keyword(s):  
Hepatocyte Proliferation ◽  
Nonparenchymal Cells ◽  
Hepatic Nonparenchymal Cells
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