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:10.1159/000217296

Cited by 12 publications

(10 citation statements)

References 1 publication

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“…It has been demonstrated that discrete cell-surface markers (ie, ␣ v ␤ 3 and E-selectin) are up-regulated in endothelial cells exposed to severe hypoxia. [51][52][53] These or similarly functioning molecules are potential candidates for the selective homing of EPCs to ischemic tissue.…”

Section: Discussionmentioning

confidence: 99%

Adult vasculogenesis occurs through in situ recruitment, proliferation, and tubulization of circulating bone marrow–derived cells

Tepper

Capla

Galiano

et al. 2005

Blood

405

318

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Ischemia is a known stimulus for vascular growth. Bone marrow (BM)-derived endothelial progenitor cells (EPCs) are believed to contribute to new blood vessel growth, but the mechanism for this contribution is unknown. To elucidate how BM cells are able to form new blood vessels, a novel murine model of soft tissue ischemia was developed in lethally irradiated mice with BM reconstituted from either tie2/lacZ or ROSA/green fluorescent protein (GFP) mice (n ‫؍‬ 24). BMderived EPCs were recruited to ischemic tissue within 72 hours, and the extent of recruitment was directly proportional to the degree of tissue ischemia. At 7 days, there were persistently elevated levels of vascular endothelial growth factor (VEGF) (2.5-fold) and circulating VEGF receptor-2/ CD11 ؊ (flk-1 ؉ /CD11 ؊ ) cells (18-fold) which correlated with increased numbers of BMderived EPCs within ischemic tissue. The cells were initially located extravascularly as proliferative clusters. By day 14, these clusters coalesced into vascular cords, which became functional vessels by day 21. In vitro examination of human EPCs from healthy volunteers (n ‫؍‬ 10) confirmed that EPC proliferation, adhesion, and chemotaxis were all significantly stimulated in hypoxic conditions. We conclude that BM-derived cells produce new blood vessels via localized recruitment, proliferation, and differentiation of circulating cells in a sequence of events markedly different from existing paradigms of angiogenesis.

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Section: Discussionmentioning

confidence: 99%

Adult vasculogenesis occurs through in situ recruitment, proliferation, and tubulization of circulating bone marrow–derived cells

Tepper

Capla

Galiano

et al. 2005

Blood

405

318

View full text Add to dashboard Cite

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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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“…In addition to modulating the pro and anticoagulant properties of the endothelium, hypoxia also up regulates the expression of P-selectin on endothelium leading to the recruitment of leukocytes or leukocyte microparticles containing tissue factor which can serve as the nidus for initiation of the thrombotic response 18,19 (Figure 2). Microparticles bearing tissue factor appear to play a role in thrombus formation 20,21 .…”

Section: A the Role Of Blood Cells Versus Vascular Contribution To Vmentioning

confidence: 99%

Basic mechanisms and pathogenesis of venous thrombosis

2009

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In 1856 Virchow proposed a triad of causes for venous thrombosis, postulating that stasis, changes in the vessel wall or changes in the blood could lead to thrombosis. We now know that abnormally high levels of some coagulation factors and defects in the natural anticoagulants contribute to thrombotic risk. Among these, factor V Leiden, which renders factor Va resistant to activated protein C, is the most prevalent with approximately 5% of the Caucasian population having this genetic alteration. These genetically controlled variants in coagulation factors work in concert with other risk factors, such as oral contraceptive use, to dramatically increase thrombotic risk. While these abnormalities in the blood coagulation proteins are associated with thrombotic disease propensity, they are less frequent contributors to thrombosis than age or cancer. Cancer increases thrombotic risk by producing tissue factor to initiate coagulation, by shedding procoagulant lipid microparticles or by impairing blood flow. Age is the strongest risk factor for thrombosis. Among possible reasons are fragility of the vessels potentially contributing to stasis, increased coagulation factor levels, impaired function of the venous valves, decreases in the efficacy of natural anticoagulants associated with the vessel wall, increased risk of immobilization and increased risk of severe infection.

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Influence Of Hypoxia And Hypoxia-Reoxygenation On Endothelial P-Selectin Expression

Cited by 12 publications

References 1 publication

Adult vasculogenesis occurs through in situ recruitment, proliferation, and tubulization of circulating bone marrow–derived cells

Adult vasculogenesis occurs through in situ recruitment, proliferation, and tubulization of circulating bone marrow–derived cells

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

Basic mechanisms and pathogenesis of venous thrombosis

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