Possible mechanism of chrysotile asbestos-stimulated superoxide anion production in guinea pig alveolar macrophages

Roney, Paul L.; Holian, Andrij

doi:10.1016/0041-008x(89)90097-5

Cited by 58 publications

(27 citation statements)

References 33 publications

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“…These observations imply that either asbestos stimulates multiple pathways and one of them is similar to that stimulated by silica, or that the particulates stimulate independent pathways. We have already described that asbestos stimulates the phospholipase C/protein kinase C pathway (14) and opens a verapamil-sensitive calcium channel in alveolar macrophages (15 Time (min) Figure 6. MAP kinase activity following endotoxin stimulation of control and silica-pretreated macrophages.…”

Section: Silica-induced Activation Of Intracellular Tyrosine Kinasesmentioning

confidence: 99%

“…Furthermore, the pathway for asbestos stimulation of alveolar macrophage superoxide anion production involves the phospholipase C/protein kinase C pathway (14) and opening of verapamil-sensitive calcium channels (15). In contrast, both chrysotile and silica stimulated cytokine release (e.g., TNF-ax and IL- 15) indicating either that the mechanism of silica stimulation was distinct from chrysotile or that chrysotile stimulated multiple pathways (16).…”

Section: Introductionmentioning

confidence: 99%

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Mechanisms associated with human alveolar macrophage stimulation by particulates.

Holian¹,

Kelley²,

Hamilton³

1994

Environ Health Perspect

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Asbestos and silica are well-known fibrogenic dusts. However, there is no comprehensive understanding of the molecular and cellular events that lead to fibrosis as a consequence of asbestos or silica inhalation. Previous studies have shown that asbestos stimulates superoxide anion production in alveolar macrophages through the phospholipase C/protein kinase C pathway. In contrast, silica does not appear to activate this pathway nor stimulate superoxide anion production, but silica does stimulate cytokine release by some undetermined pathway. Therefore, using human alveolar macrophages isolated from normal healthy volunteers, we evaluated the potential involvement of intracellular calcium and tyrosine kinases as potential signal transduction pathways. In the absence of serum, crystalline silica, and to a lesser extent amorphous silica, caused a rapid and dose-dependent elevation of intracellular calcium coming from the extracellular space. However, in the presence of serum, which is required for silica-stimulated cytokine release, neither form of silica caused noticeable elevation of intracellular calcium. Silica, however, did increase the extent of tyrosine phosphorylation, most notably of proteins at approximately 46 and 50 kDa, suggesting activation of a tyrosine kinase pathway. Preincubation of alveolar macrophages for 24 hr with silica-primed human alveolar macrophages for enhanced interleukin-1 0 (IL-1 3) release stimulated by endotoxin (LPS) that was dose dependent. The enhanced LPS-stimulated release of IL-1i correlated with enhanced mitogen-activated protein kinase activity. Taken together, these results indicate that a tyrosine kinase pathway is activated during silica stimulation of human alveolar macrophages. -Environ Health Perspect 102(Suppl 10): 69-74 (1994)

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Section: Silica-induced Activation Of Intracellular Tyrosine Kinasesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Mechanisms associated with human alveolar macrophage stimulation by particulates.

Holian¹,

Kelley²,

Hamilton³

1994

Environ Health Perspect

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“…Although the exact mechanism for the release of oxygen radicals is not clear yet, it has been accepted that asbestos stimulates oxygen radical generation by interaction with membranes of AM; the signal transduction pathway for this phenomenon also involves phospholipase C (PLC) and protein kinase C (PKC) pathways (8). PLC hydrolyzes phosphatidyl inositol biphosphate (PIP2) to diacylglycerol (DAG) and inositol triphosphate (IP3).…”

Section: Introductionmentioning

confidence: 99%

“…Asbestos stimulates the release of oxygen radicals from alveolar macrophage(s) (AM) and the generation of oxygen radicals is an important primary event in asbestos-induced cell injury (3)(4)(5)(6)(7). Among asbestos fibers, chrysotile induces the generation of oxygen radicals in AM at noncytotoxic doses whereas crocidolite and amosite do not (8). One study reports no stimulatory effect of crocidolite in AM (9), but some authors note the generation of oxygen radicals in crocidolite-stimulated AM (4,10).…”

Section: Introductionmentioning

confidence: 99%

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Involvement of protein kinase C, phospholipase C, and protein tyrosine kinase pathways in oxygen radical generation by asbestos-stimulated alveolar macrophage.

Lim

Kim

et al. 1997

Environ Health Perspect

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Although asbestos stimulates oxygen radical generation in alveolar macrophages, the exact mechanism is still not clear. The purpose of this study was to compare the ability of three asbestos fibers (amosite, chrysotile, and crocidolite) to generate oxygen radicals in macrophages and examine the mechanism of this action. All asbestos fibers were able to induce chemiluminescence but chrysotile induced maximal chemiluminescence at higher concentrations than amosite and crocidolite. Protein kinase C (PKC) inhibitors (sphingosine and staurosporine) suppressed the ability of asbestos to induce oxygen radical generation. Phospholipase C (PLC) inhibitors (U73122 and neomycin) and protein tyrosine kinase (PTK) inhibitors (erbstatin and genistein) decreased oxygen radical generation of asbestos-stimulated alveolar macrophages. Oxygen radical generation was not suppressed by an adenylate cyclase activator (forskolin), a protein kinase A inhibitor (H-8), and a protein serine-threonine phosphatase inhibitor (okadaic acid). PLC and PTK inhibitors suppressed the increment of phosphoinositide turnover by amosite. These results suggest that asbestos fibers induce the generation of oxygen radicals through PTK, PLC, and PKC pathways in a dose-response pattern.

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Cytokine and Free Radical Responses of Alveolar Macrophages in Vitro to Asbestos Fibres

2000

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Possible mechanism of chrysotile asbestos-stimulated superoxide anion production in guinea pig alveolar macrophages

Cited by 58 publications

References 33 publications

Mechanisms associated with human alveolar macrophage stimulation by particulates.

Mechanisms associated with human alveolar macrophage stimulation by particulates.

Involvement of protein kinase C, phospholipase C, and protein tyrosine kinase pathways in oxygen radical generation by asbestos-stimulated alveolar macrophage.

Cytokine and Free Radical Responses of Alveolar Macrophages in Vitro to Asbestos Fibres

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