?2-Macroglobulin secretion enhanced in rat hepatocytes by partially characterized factor from Kupffer cells

Inflammation ◽  
1985 ◽  
Vol 9 (2) ◽  
pp. 201-209 ◽  
Author(s):  
Yasuhiko Hirata ◽  
Hiromi Ishibashi ◽  
Harumichi Kimura ◽  
Kazuhiro Hayashida ◽  
Masanori Nagano ◽  
...  
2001 ◽  
Vol 120 (5) ◽  
pp. A356-A356
Author(s):  
T KONO ◽  
J IWAMOTO ◽  
K ISHIKAWA ◽  
Y EBISAWA ◽  
T AOKI ◽  
...  

1992 ◽  
Vol 73 (2) ◽  
pp. S136-S141 ◽  
Author(s):  
R. N. Racine ◽  
S. M. Cormier

Hepatic tissue from flight, synchronous, vivarium, and tail-suspended rats was examined by light microscopy and computer-assisted image analysis. Glycogen levels in flight rats were found to be significantly elevated over those in controls. Lipid was also higher but not significantly different. Hepatocytes appeared larger in flight animals because of area attributed to increased glycogen. Sinusoids were less prominent in flight animals than in controls. The total Kupffer cell population appeared to be reduced in flight animals and may represent changes in defensive capacity of the liver. Alterations in the storage of glycogen and number of Kupffer cells suggest an important effect of spaceflight on the function of the liver that may have important implications for long-term spaceflight.


1996 ◽  
Vol 315 (2) ◽  
pp. 385-392 ◽  
Author(s):  
Rainer SCHREIBER ◽  
Fan ZHANG ◽  
Dieter HÄUSSINGER

Short-term-cultivated rat hepatocytes and Kupffer cells were allowed to endocytose fluorescein isothiocyanate (FITC)-coupled dextran, in order to study the effects of aniso-osmotic exposure and NH4Cl on apparent vesicular pH (pHves) by single-cell fluorescence. Following a 2 h loading period with FITC–dextran in normo-osmotic (305 mosmol/l) medium, the apparent pHves was 6.01±0.05 (n = 39) in parenchymal cells and 4.94±0.04 (n = 76) in Kupffer cells. Under these conditions pHves in parenchymal cells, but not in Kupffer cells, was sensitive to changes in ambient osmolarity. Inhibition of vacuolar H+-ATPase by concanamycin A did not affect the osmosensitivity of pHves in parenchymal cells. However, the effects of anisotonicity on pHves were largely abolished in the presence of 4,4´-di-isothiocyanato-stilbene-2,2´-disulphonic acid (DIDS) or when extracellular chloride was substituted for gluconate. In neither Kupffer cells, nor liver parenchymal cells did hypo-osmotic cell swelling cause an increase in intracellular Ca2+. With regard to vesicular acidification, the following differences were noted between parenchymal and Kupffer cells. (1) In Kupffer cells endocytosed FITC–dextran reached a strongly acidic compartment with a pH value of approx. 5 within 5 min, whereas it took 4–5 h in parenchymal cells. Modification of pHves by hypo-osmolarity in Kupffer cells was only observed in a short-lived ‘early’ compartment with a pH value of approx. 6. (2) In contrast to pHves in parenchymal cells, pHves in Kupffer cells was very sensitive towards alkalinization by NH4Cl: addition of NH4Cl at 1 or 10 mM increased apparent pHves by 0.80 or 1.46 in Kupffer cells, but only by 0.18 or 0.56 in parenchymal cells. The low ammonia sensitivity of pHves in parenchymal cells was observed not only in the less acidic (pH approx. 6) endocytotic compartment which is reached by FITC–dextran within 2 h, but also in the stronger acidic compartment (pH approx. 5) which is reached after 4–5 h. (3) NH4Cl had no effect on the osmosensitivity of pHves in parenchymal cells, whereas in Kupffer cells pHves became sensitive to anisotonicity when NH4Cl was present. Osmosensitivity of pHves in Kupffer cells under these conditions, however, was not affected by genistein, DIDS or colchicine, whereas these compounds abolished the osmosensitivity of pHves in parenchymal cells. It is suggested that regulation of pHves by cell volume in liver parenchymal cells involves changes of vesicular chloride conductance. In addition, there are marked differences between Kupffer and parenchymal cells with respect to vesicular ammonia permeability and the kinetics of endocytotic membrane flow and acidification.


2009 ◽  
Vol 37 (2) ◽  
pp. 209-217 ◽  
Author(s):  
Yang Fan ◽  
Toshiyuki Yamada ◽  
Takeshi Shimizu ◽  
Naoki Nanashima ◽  
Miki Akita ◽  
...  

2001 ◽  
Vol 120 (5) ◽  
pp. A356
Author(s):  
Toru Kono ◽  
Jun Iwamoto ◽  
Kazushi Ishikawa ◽  
Yosiaki Ebisawa ◽  
Takanori Aoki ◽  
...  

1978 ◽  
Vol 81 (3) ◽  
pp. 1047-1053 ◽  
Author(s):  
F.Scott Furbish ◽  
Clifford J. Steer ◽  
John A. Barranger ◽  
E.Anthony Jones ◽  
Roscoe O. Brady

1978 ◽  
Vol 74 (5) ◽  
pp. 1156
Author(s):  
C.J. Steer ◽  
F.S. Furbish ◽  
J.A. Barranger ◽  
R.O. Brady ◽  
E.A. Jones

1970 ◽  
Vol 44 (3) ◽  
pp. 513-529 ◽  
Author(s):  
Sidney Goldfischer ◽  
Alex B. Novikoff ◽  
Arline Albala ◽  
Luis Biempica

The peroxidatic activity of hemoglobin permitted visualization of its uptake by rat hepatocytes by means of the Graham-Karnovsky 3,3'-diaminobenzidine (DAB) procedure. Lysosomes were visualized by their acid phosphatase, ß-glucuronidase, and glucosaminidase activities. When large doses of rat, cow, or human hemoglobin are intravenously injected, or when hemoglobinemia is induced by injection of distilled water, DAB-positive hemoglobin is engulfed by pinocytosis. Pinocytotic vacuoles become digestive vacuoles ("phagolysosomes") by fusion with lysosomes of the dense body type that have moved from their pericanalicular position. By 16–24 hr after even massive amounts of hemoglobin (400 mg/100 g), the protein is barely demonstrable in hepatocytes. At the lowest doses of injected hemoglobin (15 mg/100 g body weight), DAB-positive vacuoles are demonstrable only in the Kupffer cells.


1995 ◽  
Vol 269 (4) ◽  
pp. G518-G523 ◽  
Author(s):  
J. J. Maher

Interleukin-8 is a neutrophil chemoattractant that has been implicated in the pathogenesis of alcoholic hepatitis. The mechanism of ethanol-induced interleukin-8 production in liver is uncertain, although hepatocytes and Kupffer cells have both been proposed as sources of the chemokine. In this study we investigated whether short-term ethanol exposure stimulates production of rat interleukin-8 [cytokine-induced neutrophil chemoattractant (CINC)] by normal rat hepatocytes and Kupffer cells in primary culture. Initial experiments verified that hepatocytes and Kupffer cells produce CINC in response to cytokines or lipopolysaccharide. Ethanol, by contrast, failed to stimulate CINC secretion by either cell type even at concentrations as high as 100 mM. Although ethanol had no direct effect on liver cell CINC production, conditioned medium from ethanol-treated hepatocytes induced a threefold rise in CINC production by Kupffer cells. The increase was abrogated when hepatocytes were treated with ethanol and the metabolic inhibitor 4-methylpyrazole. The results suggest that the mechanism of ethanol-induced CINC production is indirect, involving ethanol oxidation and communication between hepatocytes and Kupffer cells.


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