Influence of Hypoxia and Hypoxia-Reoxygenation on Endothelial P-Selectin Expression

Closse, C.; Seigneur, M.; Renard, Martine; Pruvost, Annie; Dumain, Patrice; Belloc, Françis; Boisseau, M. R.

doi:10.1016/s0049-3848(96)00233-2

Cited by 40 publications

(21 citation statements)

References 20 publications

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“…These include IL-6 and TNF-a, which can be found in blood during ischemia-hypoxia of the heart (Yamauchi-Takihara et al 1995). When subjected to hypoxia and re-oxygenation, endothelial cells can produce oxygen metabolites such as superoxide anions which can induce Psel expression (Baeurele and Baltimore 1996) by activating NF-jB (Closse et al 1997). In addition, hemodynamic changes taking place during infarction are also known to affect the gene expression of adhesion molecules (Resnick and Gimbrone 1995;Malek et al 1999).…”

Section: Discussionmentioning

confidence: 99%

Upregulation of coronary endothelial P-selectin in a monkey heart ischemia reperfusion model

et al. 2010

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The design of targeted ultrasound contrast agents for molecular imaging of myocardial ischemia-reperfusion (IR) requires the availability of an adequate in vivo model in a species in which cross reactivity with the target occurs. P-selectin (Psel) is an activation-dependent endothelial receptor that supports rapid and reversible cell adhesion in a flowing system. Together with E- and L-selectins it constitutes the selectin family of adhesion molecules. We investigated the myocardial expression of selectins in a closed chest minimally invasive monkey myocardial IR model. Catheter-based occlusion (30-50 min) followed by reperfusion (3 or 5 h) of left anterior descending artery (LAD) was performed in anesthetised monkeys. At the end of each procedure animals were killed, and their hearts were excised. The tissues were analyzed immunohistochemically using an anti-human Psel antibody (AK-6 clone) that cross reacts with rhesus monkey. Histopathological features confirm the presence of IR injuries in myocardial tissues. There was significant increase in the Psel expression in vessels from the IR areas. However, significantly higher Psel immunoreactivity was also seen in areas which are distant from IR injuries.

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Section: Discussionmentioning

confidence: 99%

Upregulation of coronary endothelial P-selectin in a monkey heart ischemia reperfusion model

et al. 2010

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“…In our study, we confirmed the observation that a relatively brief period of hypoxia followed by reoxygenation elicits a significant increase in P-selectin at the endothelial surface of saphenous vein. 35 However, vein segments from a patient under statin treatment expressed significantly less P-selectin on the endothelial surface after 50 minutes of hypoxia followed by reperfusion, with a beneficial effect on leucocyteendothelial interactions compared with controls. This effect was not related to the cholesterol lowering effect of simvastatin, as it was also manifested in group B patients who did not benefit from simvastatin treatment in terms of reduced cholesterol.…”

Section: Modulation Of Neutrophil-endothelial Interactions By Statinsmentioning

confidence: 90%

Simvastatin attenuates leucocyte-endothelial interactions after coronary revascularisation with cardiopulmonary bypass

Chello

Mastroroberto²,

Patti³

et al. 2003

Heart

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Objective: To investigate the effects of preoperative simvastatin treatment on leucocyte-endothelial interactions following coronary artery bypass surgery with cardiopulmonary bypass. Design: Double blind crossover study. Experiments on polymorphonuclear cells (neutrophils) were done at the end of cardiopulmonary bypass and one hour postoperatively. Endothelial P-selectin expression and neutrophil/endothelial adhesion were evaluated under either normoxic or hypoxic conditions. Setting: University hospital (tertiary referral centre). Patients: Three groups of patients undergoing coronary bypass surgery: 20 patients taking simvastatin for cholesterol control, 16 patients not responsive to simvastatin, and 20 controls. Main outcome measures: Expression of neutrophil CD11b and endothelial P-selectin; adhesion of neutrophils to endothelium. Results: Cardiopulmonary bypass resulted in a significant increase in neutrophil CD11b expression in all groups. Similarly, the exposure of saphenous vein to hypoxia/reoxygenation induced an augmentation of endothelial P-selectin. However, both neutrophil CD11b expression and endothelial P-selectin exocytosis were less in the simvastatin groups than in the controls. Cardiopulmonary bypass and controlled hypoxia/reoxygenation stimulated neutrophil/endothelial adhesion, but the number of adhering cells was less in the simvastatin groups than in the controls, irrespective of the cholesterol concentration. Treatment of endothelial cells with L-NAME completely reversed the effects of simvastatin. Conclusions: Pretreatment with simvastatin reduces neutrophil adhesion to the venous endothelium in patients undergoing coronary surgery, irrespective of its efficacy at lowering cholesterol concentration.

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“…Subsequently, the cells have been labeled in suspension with antibodies against adhesion molecules and analyzed without fixation (8,10) or after a brief fixation with formaldehyde (7). Alternatively, the monolayers have been labeled before dissociation with trypsin/EDTA (12) or only with EDTA (13). So far, only the surface expression of endothelial adhesion molecules has been determined by flow cytometry.…”

mentioning

confidence: 99%

Flow cytometric determination of E-selectin, vascular cell adhesion molecule-1, and intercellular cell adhesion molecule-1 in formaldehyde-fixed endothelial cell monolayers

2000

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Influence of Hypoxia and Hypoxia-Reoxygenation on Endothelial P-Selectin Expression

Cited by 40 publications

References 20 publications

Upregulation of coronary endothelial P-selectin in a monkey heart ischemia reperfusion model

Upregulation of coronary endothelial P-selectin in a monkey heart ischemia reperfusion model

Simvastatin attenuates leucocyte-endothelial interactions after coronary revascularisation with cardiopulmonary bypass

Flow cytometric determination of E-selectin, vascular cell adhesion molecule-1, and intercellular cell adhesion molecule-1 in formaldehyde-fixed endothelial cell monolayers

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