Modulation of phagocytosis by anisoosmolarity and betaine in rat liver macrophages (Kupffer cells) and RAW 264.7 mouse macrophages

The role of myo-inositol as an osmolyte was studied in cultured rat liver macrophages (Kupffer cells). Hyperosmotic exposure of Kupffer cells stimulated myo-inositol uptake and led to an increase in the mRNA levels for the sodium/myo-inositol co-transporter (SMIT). Conversely, hypo-osmotic (205 m-osM) exposure diminished myo-inositol uptake when compared with normo-osmotic (305 m-osM) control incubations. The hyperosmolarity-induced SMIT mRNA increase was counteracted by added myo-inositol or betaine. In contrast with Kupffer cells, there was only a slight hyperosmotic stimulation of myo-inositol uptake in RAW 264.7 mouse macrophages, and the myo-inositol transporter (SMIT) mRNA was not detectable. Further, a slight stimulation of taurine uptake and an increase in taurine transporter (TAUT) mRNA level by hyperosmolarity was observed in RAW 264.7 cells, whereas hypo-osmolarity led to a decrease in taurine uptake and TAUT mRNA level. When Kupffer cells were preloaded with myo-inositol, hypo-osmotic exposure led to a rapid efflux of myo-inositol from the cells. Myo-inositol efflux was also stimulated by phagocytosis of latex particles; however, latex was without effect on the hyperosmolarity-induced increase of SMIT mRNA levels. The results suggest a role of myo-inositol as an osmolyte in rat Kupffer cells but not in RAW 264.7 mouse macrophages. The functional relevance of this osmolyte strategy might lie in the maintenance of cell volume homeostasis during phagocytosis in Kupffer cells; however, the interplay with the other osmolytes betaine and taurine remains to be established.

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Identification of betaine as an osmolyte in rat liver macrophages (Kupffer cells)

Gastroenterology ◽

10.1053/gast.1996.v110.pm8613062 ◽

1996 ◽

Vol 110 (5) ◽

pp. 1543-1552 ◽

Cited By ~ 61

Author(s):

F Zhang ◽

U Warskulat ◽

M Wettstein ◽

D Haussinger

Keyword(s):

Rat Liver ◽

Kupffer Cells ◽

Liver Macrophages

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Modulation of tumor necrosis factor-α release by anisoosmolarity and betaine in rat liver macrophages (Kupffer cells)

FEBS Letters ◽

10.1016/0014-5793(96)00754-5 ◽

1996 ◽

Vol 391 (3) ◽

pp. 293-296 ◽

Cited By ~ 31

Author(s):

Fan Zhang ◽

Ulrich Warskulat ◽

Dieter Häussinger

Keyword(s):

Tumor Necrosis Factor ◽

Rat Liver ◽

Kupffer Cells ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Liver Macrophages ◽

Factor Α ◽

Necrosis Factor

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[64] Isolation of adult rat liver macrophages (Kupffer cells)

Biomembranes Part B - Methods in Enzymology ◽

10.1016/0076-6879(74)32067-8 ◽

1974 ◽

pp. 647-653 ◽

Cited By ~ 3

Author(s):

P.E. Lentz ◽

N.R. Di Luzio

Keyword(s):

Rat Liver ◽

Kupffer Cells ◽

Adult Rat ◽

Liver Macrophages

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Inhibitory Effect of (4R)-Hexahydro-7,7-Dimethyl-6-Oxo-l,2,5-Dithiazocine-4-Carboxylic Acid (SA3443), a Novel Cyclic Disulfide, on the Production of TNF-Like Factor from Propionibacterium Acnes-Primed Rat Liver Macrophages/Kupffer Cells

The Japanese Journal of Pharmacology ◽

10.1254/jjp.59.493 ◽

1992 ◽

Vol 59 (4) ◽

pp. 493-496 ◽

Cited By ~ 2

Author(s):

Minoru Sasano ◽

Katsuhiko Nakata ◽

Shiro Mita

Keyword(s):

Carboxylic Acid ◽

Rat Liver ◽

Kupffer Cells ◽

Propionibacterium Acnes ◽

Inhibitory Effect ◽

Liver Macrophages

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Hyperosmolarity stimulates prostaglandin synthesis and cyclooxygenase-2 expression in activated rat liver macrophages

Biochemical Journal ◽

10.1042/bj3120135 ◽

1995 ◽

Vol 312 (1) ◽

pp. 135-143 ◽

Cited By ~ 55

Author(s):

F Zhang ◽

U Warskulat ◽

M Wettstein ◽

R Schreiber ◽

H P Henninger ◽

...

Keyword(s):

Rat Liver ◽

Kupffer Cells ◽

Critical Factor ◽

Pge2 Production ◽

Mrna Levels ◽

Dependent Manner ◽

Liver Macrophages ◽

Prostanoid Production ◽

Cox 2 ◽

Stimulation Of

The effect of aniso-osmotic exposure on the level of inducible cyclooxygenase (Cox-2) and on prostanoid synthesis was studied in cultured rat liver macrophages (Kupffer cells). In lipopolysaccharide (LPS)- or phorbol 12-myristate 13-acetate-stimulated Kupffer cells, hyperosmotic (355 mosmol/l) exposure, due to addition of NaCl or impermeant sugars, markedly increased prostaglandin (PG) E2, D2 and thromboxane B2 synthesis in a time- and osmolarity-dependent manner. Increased prostanoid production was observed about 8 h after exposure to LPS in hyperosmotic medium compared to Kupffer cells treated with LPS under normotonic (305 mosmol/l) conditions. A similar stimulatory effect of hyperosmolarity on PGE2 production was also seen when arachidonate was added exogenously. Hyperosmotic stimulation of PGE2 production was accompanied by a strong induction of Cox-2 mRNA levels and an increase in immunoreactive Cox-2, whereas the levels of immunoreactive phospholipase A2 and cyclooxygenase-1 did not change significantly. Dexamethasone, indomethacin and the selective Cox-2 inhibitor, NS-398, abolished the hypertonicity-induced stimulation of PGE2 formation; dexamethasone also prevented the increase in Cox-2 mRNA and protein. The increase of immunoreactive Cox-2 lasted for about 24 h and was also blocked by actinomycin D or cycloheximide, but not by brefeldin A. Tunicamycin or treatment with endoglucosidase H reduced the molecular mass of hypertonicity-induced Cox-2 by 5 kDa. Tunicamycin treatment also suppressed the hypertonicity-induced stimulation of PGE2 production. The hyperosmolarity/LPS-induced stimulation of prostaglandin formation was partly sensitive to protein kinase C inhibition but was not accompanied by an increase in the cytosolic free Ca2+ concentration. The data suggest that osmolarity may be a critical factor in the regulation of Cox-2 expression and prostanoid production in activated rat liver macrophages.

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