Abstract:
:Cytokine activation of vascular endothelial cells renders the hyperadhesiveness for neutrophils. During the processes of inflammation and atherosclerosis, the production of reactive oxygen species by neutrophils contributes to endothelial cell (EC) damage and injury. However, the precise mechanisms for neutrophil activation by ECs remain unknown. Thus, we investigated what kinds of pathophysiological factors synthesized by inflammatory cytokine-activated ECs potentiated the activity of neutrophil functions. The magnitude of O(2)(-) release from neutrophils, which is one of pivotal neutrophil functions, was measured as an indicator potentiated by activated ECs. Neutrophils release massive amounts of O(2)(-) on coculture with activated ECs. Anti-granulocyte-macrophage colony-stimulating factor (GM-CSF) antibody (Ab) or specific platelet-activating factor (PAF)-receptor antagonist suppressed the O(2)(-) release from neutrophils on coculture with the activated ECs by 50% to 70%. The supernatants from activated ECs also induced O(2)(-) release by neutrophils. This stimulatory effect of activated EC supernatants on O(2)(-) release by neutrophils was abolished by anti-GM-CSF Ab or by PAF-receptor antagonist. As we previously reported, we demonstrated the expression of GM-CSF mRNA by Northern blotting and protein synthesis of GM-CSF by ELISA on tumor necrosis factor as well as interleukin-1-activated ECs. Although phosphorylation of mitogen-activated protein kinases was observed in ECs stimulated by tumor necrosis factor and interleukin-1, treatment of ECs with PD98059 (MEK1 inhibitor) and SB203580 (p38 mitogen-activated protein kinase inhibitor) in the presence of the cytokine failed to attenuate the stimulatory effect of activated ECs on neutrophil activation. We found that activated ECs regulated neutrophil function on coculture. We show here for the first time, to our knowledge, that the collaboration between GM-CSF and PAF synthesized by activated ECs markedly potentiated neutrophil activation.
journal_name
Circ Resjournal_title
Circulation researchauthors
Takahashi T,Hato F,Yamane T,Fukumasu H,Suzuki K,Ogita S,Nishizawa Y,Kitagawa Sdoi
10.1161/01.res.88.4.422subject
Has Abstractpub_date
2001-03-02 00:00:00pages
422-9issue
4eissn
0009-7330issn
1524-4571journal_volume
88pub_type
杂志文章abstract::During an investigation of the effect of ryanodine on contractions in cardiac muscle, it was found that long rest periods removed all or most of the drug's effect. Therefore, we studied the kinetics of block development and recovery from block produced by low concentrations of ryanodine (1-100 pM) on the postrest cont...
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pub_type: 杂志文章
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更新日期:1996-04-01 00:00:00
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pub_type: 杂志文章
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pub_type: 杂志文章
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pub_type: 杂志文章
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doi:10.1161/CIRCRESAHA.109.204040
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pub_type: 杂志文章
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abstract::Topical application of sodium arachidonate (50-200 micrograms/ml) or bradykinin (0.1-10 micrograms/ml) on the brain surface of anesthetized cats caused dose-dependent cerebral arteriolar dilation. This dilation was blocked by 67-100% in the presence of superoxide dismutase and catalase. These enzymes did not affect th...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.55.3.295
更新日期:1984-09-01 00:00:00
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pub_type: 杂志文章,评审
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更新日期:2019-03-29 00:00:00
abstract::An animal model was used to test the hypothesis that in heart failure the decrease in the ability to resynthesize ATP through the creatine kinase (CK) reaction (which we call energy reserve) contributes to the inability of the heart to maintain its normal function and contractile reserve. One-week-old turkey poults we...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.78.5.893
更新日期:1996-05-01 00:00:00
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pub_type: 杂志文章,评审
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更新日期:2012-04-13 00:00:00
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更新日期:2008-05-09 00:00:00
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pub_type: 杂志文章
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更新日期:1988-08-01 00:00:00