Reduced vascular endothelial growth factor correlates with alveolar epithelial damage after experimental ischemia and reperfusion

Fehrenbach, Antonia; Pufe, Thomas; Wittwer, Thorsten; Nagib, Ragi; Dreyer, Niels; Pech, Thomas; Petersen, Wolf; Fehrenbach, Heinz; Wahlers, Thorsten; Richter, Joachim

doi:10.1016/s1053-2498(02)01157-9

Cited by 30 publications

(19 citation statements)

References 37 publications

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“…On the other hand, these cells are one of the main sources of VEGF in the lung [11]. Thus, the death of alveolar epithelial cells could be partially responsible for the decreased expression of VEGF [50]. …”

Section: Discussionmentioning

confidence: 99%

The early responses of VEGF and its receptors during acute lung injury: implication of VEGF in alveolar epithelial cell survival

et al. 2006

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Section: Discussionmentioning

confidence: 99%

The early responses of VEGF and its receptors during acute lung injury: implication of VEGF in alveolar epithelial cell survival

et al. 2006

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“…Thus, a reduction in alveolar levels of VEGF is not specific for ALI/ARDS and occurs in acute pulmonary oedema regardless of the aetiology. lung, possible modulators of VEGF levels include alveolar epithelial injury [17] and hypoxic upregulation of alveolar epithelial VEGF synthesis [7]. The overall drop in VEGF levels and lack of association between VEGF levels and the degree of hypoxia suggests that hypoxic upregulation of VEGF production is probably not the predominant determinant.…”

Section: Vegf Levels and Clinical Outcomesmentioning

confidence: 99%

VEGF levels in the alveolar compartment do not distinguish between ARDS and hydrostatic pulmonary oedema

Ware

Kaner²,

Crystal³

et al. 2005

Eur Respir J

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Although overexpression of vascular endothelial growth factor (VEGF) 165 in the lung causes pulmonary oedema, its role in human acute lung injury (ALI) is unclear. VEGF levels are reported to be lower in bronchoalveolar lavage from ALI patients compared with normals, but these studies did not include a comparably ill control group with noninflammatory pulmonary oedema.The current authors hypothesised that VEGF levels in pulmonary oedema fluid would be lower in ALI patients compared with control patients with severe hydrostatic pulmonary oedema. VEGF was measured in pulmonary oedema fluid and plasma from 56 patients with ALI and 46 controls with severe hydrostatic pulmonary oedema.Pulmonary oedema fluid levels of VEGF did not differ between patients with hydrostatic oedema (median 799 pg?mL -1 , interquartile range (IQR) 226-2,281) and ALI (median 507, IQR 0.8-1,031).Plasma levels were also the same (median 20.5 pg?mL -1 , IQR 0-152 versus 4.8, IQR 0-99.8). There was no association between plasma or oedema fluid VEGF levels and outcomes including mortality. Vascular endothelial growth factor levels in pulmonary oedema fluid were depressed both in acute lung injury and hydrostatic pulmonary oedema. The decrease in air space concentrations of vascular endothelial growth factor in acute lung injury may not be a function of the degree of lung injury, but rather may result from alveolar flooding.

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“…[1][2][3] Vascular endothelial growth factor (VEGF)-C activates the endothelial cell-specific tyrosine kinase receptors VEGFR-2 and VEGFR-3. 4 Activation of VEGFR-2 by VEGF-C results in a mitogenic response and capillary endothelial cell proliferation and migration.…”

mentioning

confidence: 99%

Vascular Endothelial Growth Factor C–induced Collateral Formation in a Model of Myocardial Ischemia

Pätilä¹,

Ikonen²,

Rutanen³

et al. 2006

The Journal of Heart and Lung Transplantation

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Reduced vascular endothelial growth factor correlates with alveolar epithelial damage after experimental ischemia and reperfusion

Cited by 30 publications

References 37 publications

The early responses of VEGF and its receptors during acute lung injury: implication of VEGF in alveolar epithelial cell survival

The early responses of VEGF and its receptors during acute lung injury: implication of VEGF in alveolar epithelial cell survival

VEGF levels in the alveolar compartment do not distinguish between ARDS and hydrostatic pulmonary oedema

Vascular Endothelial Growth Factor C–induced Collateral Formation in a Model of Myocardial Ischemia

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