High and low cytosolic Ca2+ induced macrophage death?

Rooijen, Nico van

doi:10.1016/0143-4160(91)90063-k

Cited by 13 publications

(4 citation statements)

References 28 publications

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“…Freshly isolated PBLs were incubated for 10 As observed in previous experiments (Fig. 1, 3 endonucleases that are toxic to the cell (19)(20)(21). Red drum PBLs stimulated with 1 jIM HgCl2 displayed a twofold rise in fura-2 fluorescence ratio, which was remarkably similar to the kinetics and duration of calcium flux observed in mammalian lymphocytes treated in a similar fashion (22).…”

Section: Concentration and Time-dependent Effects Of Hgcl2 On Pbl Promentioning

confidence: 68%

Exposure to Mercury Alters Early Activation Events in Fish Leukocytes

MacDougal¹,

Johnson²,

Burnett³

1996

Environmental Health Perspectives

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Section: Concentration and Time-dependent Effects Of Hgcl2 On Pbl Promentioning

confidence: 68%

Exposure to Mercury Alters Early Activation Events in Fish Leukocytes

MacDougal¹,

Johnson²,

Burnett³

1996

Environmental Health Perspectives

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“…Because clodronate has a high affinity for calcium and iron, the chelation of intracellular calcium [11,12] and/or iron [5] might be the mechanism of action of the compound.…”

Section: Discussionmentioning

confidence: 99%

“…Macrophages are also physically removed from the spleen, as confirmed by ultrastructural studies [5,9]. The mechanism of macrophage elimination by liposomal clodronate is not known, but it has been suggested that the chelation of intracellular calcium [11,12] and/or iron [5] plays a crucial role in this phenomenon.…”

mentioning

confidence: 90%

The effects of liposome-encapsulated and free clodronate on the growth of macrophage-like cellsin vitro: The role of calcium and iron

Mönkkönen

Heath

1993

Calcif Tissue Int

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Clodronate (dichloromethylene bisphosphonate) inhibits the activity of osteoclasts, thereby preventing bone resorption in disorders characterized by excessive bone loss. Intravenously injected clodronate encapsulated in liposomes is also known to inactivate phagocytic cells in spleen and liver in vivo. The macrophage suppressive effect of clodronate is of interest in autoimmune diseases, like rheumatoid arthritis, in which phagocytic cells are involved in inflammatory processes, but knowledge of the interaction of clodronate with phagocytic cells is scarce. We have studied the uptake of clodronate, both free and encapsulated in negatively charged liposomes, by the macrophage-like cell line RAW 264 and by other types of cell lines. The uptake was assessed by a growth inhibition assay. The liposome-encapsulated clodronate was 50 and 350 times more potent than free drug for RAW 264 and CV1-P, respectively. Cell lines with a lower endocytotic capacity were insensitive to liposome-mediated delivery of the drug. The action of free clodronate seemed to be extracellular in all cell lines studied. Calcium and/or iron have been suggested to be involved in the intracellular uptake and action of clodronate in phagocytic cells. We found that the uptake of free clodronate by RAW 264 cells was indeed mediated by calcium and iron, while the uptake of liposomal drugs was only slightly affected by calcium. The increased intracellular calcium concentration in macrophages did not significantly affect the growth-inhibitory properties of clodronate, whereas iron loading of the cells partially restored the cell growth. The data do not support the role of calcium chelation as a mechanism of action of clodronate, but suggest that intracellular iron is, at least partially involved.

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“…Clodronate is then released in these cells by phospholipase action on liposomes. Although, the mechanism of action of clodronate is unknown, the drug might inactive macrophage phagocytosis by chelating Ca 2þ or metallic ions (Van Rooijen, 1991) or directly inducing apoptosis (Naito et al, 1996). Macrophages from different tissues can be specifically targeted depending on the route of administration; intravenous injection of liposome-encapsulated clodronate depletes mainly spleen macrophage subsets and Kupffer cells of liver; subcutaneous injection depletes draining lymph nodes (Van Rooijen and Sanders, 1994).…”

Section: Principle Of the Techniquementioning

confidence: 99%

Involvement of Macrophages in the Pathogenesis of Transmissible Spongiform Encephalopathies

Béringue

Couvreur²,

Dormont

2002

Journal of Immunology Research

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Although transmissible spongiform encephalopathies (TSE) or prion diseases are neurodegenerative disorders, the immune system is also involved, at least in the early stages of their pathogenesis. Extensive studies have focused on cells targeted by the TSE agent for its replication but few on the possible involvement of macrophages in its clearance, as in more conventional diseases. This review summarises some of the experiments aimed at demonstrating a role for macrophages in TSE and presents the application to TSE of the macrophage "suicide" technique, which has been used to clarify the implication of these cells in the early steps of TSE pathogenesis.

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High and low cytosolic Ca2+ induced macrophage death?

Cited by 13 publications

References 28 publications

Exposure to Mercury Alters Early Activation Events in Fish Leukocytes

Exposure to Mercury Alters Early Activation Events in Fish Leukocytes

The effects of liposome-encapsulated and free clodronate on the growth of macrophage-like cellsin vitro: The role of calcium and iron

Involvement of Macrophages in the Pathogenesis of Transmissible Spongiform Encephalopathies

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