Prevention of In vitro neutrophil adhesion to endothelial cells through shedding of L-selectin by C-reactive protein and peptides derived from C-reactive protein.

Zouki, Christine; Beauchamp, Marie‐Claude; Baron, Chantal; Filep, János G.

doi:10.1172/jci119561

Cited by 134 publications

(118 citation statements)

References 36 publications

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“…[17][18][19] For instance, native CRP inhibits whereas mCRP promotes adhesion of neutrophils to LPS-activated HCAECs. 11,19 Furthermore, recent results suggest that aggregated (ie, structurally modified) CRP rather than native CRP may promote uptake of low-density lipoproteins by macrophages. 26,27 To avoid the confounding effects of spon- …”

Section: Discussionmentioning

confidence: 99%

“…11 Monolayers of HCAECs (passages 4 through 6) in 24-well or 96-well microplates (confluence Ͼ97%, Ϸ28 000 cells/cm 2 ) were incubated with native CRP or mCRP. In some experiments, HCAECs were pretreated with the MAPK kinase inhibitor PD98059 (50 mol/L), the p38 MAPK inhibitor SB203580 (0.1 to 1 mol/L), the phosphatidylinositol 3-kinase inhibitor wortmannin (100 nmol/L), the anti-Fc␥RIII (CD16) antibody 3G8, anti-Fc␥RIIa (CD32) antibody FLI8.26, or the irrelevant antibody MOPC-21 (each at 2.5 g/mL, Pharmingen) for 30 minutes before addition of mCRP.…”

Section: Hcaec Stimulationmentioning

confidence: 99%

“…11,19 In brief, monolayers of HCAECs in 96-well microplates were cultured with CRP, mCRP, or LPS (1 g/mL, a positive control) for 4 hours at 37°C and washed extensively, and 2ϫ10 5 human 51 Cr-labeled neutrophils in 100 L were then added. In some experiments, mCRP was added back together with neutrophils to mCRP-treated HCAECs.…”

Section: Neutrophil-endothelial Cell Adhesion Assaymentioning

confidence: 99%

“…Because multiple receptors are involved in neutrophil adhesion to HCAECs under nonstatic conditions 11 and mCRP affects adhesion molecule expression on both neutrophils 19 and endothelial cells (the present study), we assessed the contribution of L-selectin, ␤ 2 -integrins, and E-selectin to the binding interaction by using function-blocking monoclonal antibodies. mCRP-stimulated neutrophil attachment to mCRP-activated HCAECs was blocked by antibodies against CD18 (57Ϯ4%, nϭ6), E-selectin (38Ϯ3%), and L-selectin (14Ϯ2%) ( Figure 5C).…”

Section: Mcrp Promotes Neutrophil Adhesion To Hcaecsmentioning

confidence: 99%

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Conformational Rearrangement in C-Reactive Protein Is Required for Proinflammatory Actions on Human Endothelial Cells

et al. 2004

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Background-C-reactive protein (CRP) has been suggested to actively amplify the inflammatory response underlying coronary heart diseases by directly activating endothelial cells. In this study, we investigated whether loss of the cyclic pentameric structure of CRP, resulting in formation of modified or monomeric CRP (mCRP), is a prerequisite for endothelial cell activation. Methods and Results-We examined the impact of native CRP and mCRP on the production of monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8), key regulators of leukocyte recruitment, and on the expression of intercellular adhesion molecule-1 (ICAM-1), E-selectin, and vascular adhesion molecule-1 (VCAM-1) in human cultured coronary artery endothelial cells (HCAECs). Incubation with mCRP for 4 hours increased MCP-1 and IL-8 secretion and mRNA levels and expression of ICAM-1, E-selectin, and VCAM-1 protein and mRNA. Significant induction occurred at 1 to 5 g/mL, reached a maximum at 30 g/mL, and did not require the presence of serum. Native CRP was without detectable effects at 4 hours, whereas it enhanced cytokine release after a 24-hour incubation. An anti-Fc␥RIII (CD16) but not an anti-Fc␥RII (CD32) antibody produced a 14% to 32% reduction of the mCRP effects (PϽ0.05). mCRP but not CRP evoked phosphorylation of p38 mitogen-activated protein kinase, and inhibition of this kinase with SB 203580 reversed the effects of mCRP. Furthermore, culture of HCAECs in the presence of SB203580 markedly decreased mCRP-stimulated E-selectin and ICAM-1-dependent adhesion of neutrophils to HCAECs (PϽ0.001). Conclusions-Loss of pentameric symmetry in CRP, resulting in formation of mCRP, promotes a proinflammatory HCAEC phenotype through a p38 MAPK-dependent mechanism.

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Section: Discussionmentioning

confidence: 99%

Section: Hcaec Stimulationmentioning

confidence: 99%

Section: Neutrophil-endothelial Cell Adhesion Assaymentioning

confidence: 99%

Section: Mcrp Promotes Neutrophil Adhesion To Hcaecsmentioning

confidence: 99%

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Conformational Rearrangement in C-Reactive Protein Is Required for Proinflammatory Actions on Human Endothelial Cells

et al. 2004

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“…CRP has anti-inflammatory roles as well. For instance, one study demonstrated that increased CRP levels caused a detachment of Lselectin thereby decreasing endothelial neutrophil adhesion (Zouki et al 1997). …”

Section: C-reactive Protein (Crp)mentioning

confidence: 99%

Homocysteine and Malondialdehyde as Predictors of Restenosis Following Percutaneous Coronary Intervention

et al. 2006

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Restenosis is one of the major adverse outcomes of Percutaneous CoronaryIntervention (PCI). Previous studies have shown conflicting reports for homocysteine as a predictor of restenosis following PCI. The conflicting reports may be due to oxidative factors (stimulation of polymorphonuclear leukocyte [PMNL]-induced reactive oxygen species generation, xanthine-xanthine oxidase, and arachidonic acid metabolism) other than homocysteine which could cause endothelial cell dysfunction leading to restenosis.Malondialdehyde (MDA), a lipid peroxidation product, is a marker for oxidative stress and is related to all oxidative factors. Therefore, it is possible that serum MDA may be a better predictor of restenosis than plasma homocysteine. The purpose of this study is to determine whether or not the pre-procedural serum MDA and plasma homocysteine levels are elevated in patients who develop restenosis post PCI.The study included fifty-one patients undergoing elective PCI who consented to participate in a protocol that was approved by the Ethics Committee of the University of Saskatchewan. Homocysteine and malondialdehyde were measured in the plasma and serum respectively. Blood samples were collected pre-procedural, 0 time, 8 hours, 24 hours, and 6 months post-procedure. Exercise tolerance tests were performed at two weeks, and six months post-procedure to determine if there was any evidence of restenosis.The results of the study showed that pre-procedural values of plasma homocysteine in the restenosis and non-restenosis groups were 10.37 ± 0.46 and 10.73 ± 0.49 respectively. These values were not significantly different (p=0.60) between the groups. The pre-procedural levels of plasma homocysteine were not significantly ii different (p=0.08) from the post-PCI values of those patients who did not develop restenosis at the 6-month time interval. However, the pre-procedural levels of plasma homocysteine were significantly different from the post-PCI values of those patients in the restenosis group at the 24hr (p=0.04) and 6-month (p=0.002) time intervals. In the restenosis group there was a significant increase (24%) after six months in the values of homocysteine from the pre-procedural levels. Thus, this indicates that restenosis is associated with higher post-PCI levels of homocysteine.The pre-procedural levels of serum MDA in the restenosis and non-restenosis groups were 0.124± 0.16 and 0.147± 0.02 respectively. There was no significant difference (p=0.60) between the two groups. There was also no significant difference The results suggest that pre-procedural levels of plasma homocysteine and serum MDA were not predictors of restenosis following PCI. However, the post-PCI sixmonth levels of both homocysteine and MDA are predictors of restenosis. Moreover, the post-PCI levels of MDA were better predictors of restenosis than the post-PCI levels of homocysteine because the increase in MDA levels were greater at six months than the rise in homocysteine levels at the same time interval.iii ACKNOWLEDGEMENTS

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C‐Reactive Protein

Volanakis

2002

Wiley Encyclopedia of Molecular Medicine

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Prevention of In vitro neutrophil adhesion to endothelial cells through shedding of L-selectin by C-reactive protein and peptides derived from C-reactive protein.

Cited by 134 publications

References 36 publications

Conformational Rearrangement in C-Reactive Protein Is Required for Proinflammatory Actions on Human Endothelial Cells

Conformational Rearrangement in C-Reactive Protein Is Required for Proinflammatory Actions on Human Endothelial Cells

Homocysteine and Malondialdehyde as Predictors of Restenosis Following Percutaneous Coronary Intervention

C‐Reactive Protein

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