Faculty Opinions recommendation of An unbiased stereological study on subpopulations of rat liver macrophages and on their numerical relation with the hepatocytes and stellate cells.

2009 ◽  
Author(s):  
Ralf Weiskirchen ◽  
Jens Herrmann
Keyword(s):  
Rat Liver ◽  
Stellate Cells ◽  
Liver Macrophages ◽  
Numerical Relation

scholarly journals An unbiased stereological study on subpopulations of rat liver macrophages and on their numerical relation with the hepatocytes and stellate cells

2009 ◽  
Vol 214 (5) ◽  
pp. 744-751 ◽  
Author(s):  
Marta Santos ◽  
Ricardo Marcos ◽  
Nádia Santos ◽  
Fernanda Malhão ◽  
Rogério A. F. Monteiro ◽  
...  
Keyword(s):  
Rat Liver ◽  
Stellate Cells ◽  
Liver Macrophages ◽  
Numerical Relation

Inhibition of PDGF signaling promotes hepatic differentiation of stellate cells from rat liver

2018 ◽  
Vol 56 (01) ◽  
pp. E2-E89
Author(s):  
D Reichert ◽  
L Adolph ◽  
J Köhler ◽  
C Kordes ◽  
D Häussinger
Keyword(s):  
Rat Liver ◽  
Stellate Cells ◽  
Hepatic Differentiation ◽  
Pdgf Signaling

scholarly journals Portal hypertensive response to kinin

2009 ◽  
Vol 81 (3) ◽  
pp. 431-442 ◽  
Author(s):  
Maria Kouyoumdjian ◽  
Marcia R. Nagaoka ◽  
Mauricio R. Loureiro-Silva ◽  
Durval R. Borges
Keyword(s):  
Vascular Resistance ◽  
Rat Liver ◽  
Liver Perfusion ◽  
Stellate Cells ◽  
Kinin System ◽  
Rat Liver Perfusion ◽  
Isolated Liver Cells ◽  
B2 Receptors ◽  
Intrahepatic Vascular Resistance

Portal hypertension is the most common complication of chronic liver diseases, such as cirrhosis. The increased intrahepatic vascular resistance seen in hepatic disease is due to changes in cellular architecture and active contraction of stellate cells. In this article, we review the historical aspects of the kallikrein-kinin system, the role of bradykinin in the development of disease, and our main findings regarding the role of this nonapeptide in normal and experimentalmodels of hepatic injury using the isolated rat liver perfusion model (mono and bivascular) and isolated liver cells. We demonstrated that: 1) the increase in intrahepatic vascular resistance induced by bradykinin is mediated by B2 receptors, involving sinusoidal endothelial and stellate cells, and is preserved in the presence of inflammation, fibrosis, and cirrhosis; 2) the hepatic arterial hypertensive response to bradykinin is calcium-independent and mediated by eicosanoids; 3) bradykinin does not have vasodilating effect on the pre-constricted perfused rat liver; and, 4) after exertion of its hypertensive effect, bradykinin is degraded by angiotensin converting enzyme. In conclusion, the hypertensive response to BK is mediated by the B2 receptor in normal and pathological situations. The B1 receptor is expressed more strongly in regenerating and cirrhotic livers, and its role is currently under investigation.

Hepatic Stellate Cells Play a Functional Role in Exacerbating Ischemia-Reperfusion Injury in Rat Liver

2019 ◽  
Vol 60 (1-2) ◽  
pp. 74-85 ◽  
Author(s):  
Tomokazu Takahashi ◽  
Masato Yoshioka ◽  
Hiroshi Uchinami ◽  
Yasuhiko Nakagawa ◽  
Naohiko Otsuka ◽  
...  
Keyword(s):  
Rat Liver ◽  
Hepatic Stellate Cells ◽  
Functional Role ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Stellate Cells ◽  
Treated Group ◽  
Sprague Dawley ◽  
Perfusion Rate ◽  
Sprague Dawley Rats

Purpose: The involvement of hepatic stellate cells (HSCs) with ischemia-reperfusion (I/R) injury in rat liver was examined using gliotoxin, which is known to induce HSC apoptosis. Methods: Male Sprague-Dawley rats were used. HSC was represented by a glial fibrillary acidic protein (GFAP)-positive cell. Liver ischemia was produced by cross-clamping the hepatoduodenal ligament. The degree of I/R injury was evaluated by a release of aminotransferases. Sinusoidal diameter and sinusoidal perfusion rates were examined using intravital fluorescence microscopy. Results: Gliotoxin significantly decreased the number of GFAP-positive cells 48 h after dosing (2.50 ± 0.19% [mean ± SD] in the nontreated group vs. 1.91 ± 0.46% in the gliotoxin-treated group). Liver damage was significantly suppressed by the pretreatment with gliotoxin. Sinusoidal diameters in zone 3 were wider in the gliotoxin group (10.25 ± 0.35 µm) than in the nontreated group (8.21 ± 0.50 µm). The sinusoidal perfusion rate was maintained as well in the gliotoxin group as in normal livers, even after I/R. Conclusions: Pretreatment with gliotoxin significantly reduced the number of HSCs in the liver and further suppressed liver injury following I/R. It is strongly suggested that HSCs play a functional role in exacerbating the degree of I/R injury of the liver.

scholarly journals Differential regulation of TGF-β signal in hepatic stellate cells between acute and chronic rat liver injury

Hepatology ◽  
2002 ◽  
Vol 35 (1) ◽  
pp. 49-61 ◽  
Author(s):  
Yoshiya Tahashi ◽  
Koichi Matsuzaki ◽  
Masataka Date ◽  
Katsunori Yoshida ◽  
Fukiko Furukawa ◽  
...  
Keyword(s):  
Liver Injury ◽  
Rat Liver ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Differential Regulation

Rat liver myofibroblasts and hepatic stellate cells: Different cell populations of the fibroblast lineage with fibrogenic potential

1999 ◽  
Vol 117 (5) ◽  
pp. 1205-1221 ◽  
Author(s):  
Thomas Knittel ◽  
Dominik Kobold ◽  
Bernhard Saile ◽  
Anka Grundmann ◽  
Katrin Neubauer ◽  
...  
Keyword(s):  
Rat Liver ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Cell Populations ◽  
Liver Myofibroblasts
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