Lung Overexpression of the Vascular Endothelial Growth Factor Gene Induces Pulmonary Edema

Kaner, Robert J.; Ladetto, John V.; Singh, Ravi; Fukuda, Norimasa; Matthay, Michael A.; Crystal, Ronald G.

doi:10.1165/ajrcmb.22.6.3779

Cited by 259 publications

(238 citation statements)

References 46 publications

(58 reference statements)

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“…Thus, a role for VEGF in the initial increase in endothelial permeability that characterises ARDS cannot be excluded. In keeping with this possibility, adenoviral-induced overexpression of VEGF in healthy animals is associated with increased oedema formation [19]. Interestingly, in the present study, VEGF immunolocalisation labelled alveolar inflammatory cells, in agreement with the finding by THICKETT et al [6], which demonstrated that VEGF was released by isolated inflammatory cells.…”

Section: Vascular Endothelial Growth Factor and Ards Y Abadie Et Alsupporting

confidence: 93%

Decreased VEGF concentration in lung tissue and vascular injury during ARDS

Abadie

Brégeon²,

Papazian³

et al. 2005

European Respiratory Journal

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Endothelial injury is an important prognostic factor in acute respiratory distress syndrome (ARDS). Decreased production of vascular endothelial growth factor (VEGF) in ARDS may favour vascular lesions, since VEGF promotes endothelial survival by inhibiting apoptosis.This study sought to document low VEGF levels in lung tissue from ARDS patients, to determine whether the cause was injury to alveolar type II cells (the main pulmonary source of VEGF) and to evaluate the vascular consequences. Lung specimens were obtained by open biopsy or autopsy from 29 patients with severe ARDS (two survivors) and five controls.As compared with controls, homogenates of lung tissue from ARDS patients contained less VEGF (median (interquartile range) ARDS 8.2 (4.7-12.2) versus controls 28.4 (9.9-47.1) ng?g -1 protein). Increased immunostaining with surfactant protein B was seen in ARDS lungs. Extensive cellular apoptosis (terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labelling staining), including endothelial and alveolar type II cells, was demonstrated, and vascular bed density (CD31 immunostaining) decreased in ARDS lungs as compared with controls. VEGF levels were negatively correlated to apoptotic endothelial cell counts.In conclusion, decreased vascular endothelial growth factor levels in lung tissue may participate in the decrease in lung perfusion in acute respiratory distress syndrome.

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Section: Vascular Endothelial Growth Factor and Ards Y Abadie Et Alsupporting

confidence: 93%

Decreased VEGF concentration in lung tissue and vascular injury during ARDS

Abadie

Brégeon²,

Papazian³

et al. 2005

European Respiratory Journal

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“…15,16 Disruption of the alveolar-capillary membrane leads to flooding of the alveoli, causing disturbances in pulmonary mechanics and impairment of gas exchange. 17,18 Multiple investigators have confirmed the similarities in the stages and morphologic patterns of pulmonary oxygen toxicity in many animal species as well as man. 19 …”

Section: Introductionmentioning

confidence: 94%

The Role of Angiopoietin 2 in Hyperoxia-Inuduced Acute Lung Injury

Bhandari¹,

Elias²

2007

Cell Cycle

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“…The EB concentration was expressed as a percentage of the total dose of EB administered as described earlier. 16 …”

Section: Ebmentioning

confidence: 99%

Resolvin D1 reduces deterioration of tight junction proteins by upregulating HO-1 in LPS-induced mice

Xie

Wang

et al. 2013

Laboratory Investigation

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Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) is characterized by increased pulmonary permeability with high mortality. Resolvin D1 (RvD1), which has potent anti-inflammatory and pro-resolving activity, can attenuate pulmonary edema in the animal model of ALI. However, the mechanism underlying the protection of RvD1 on pulmonary edema is still unknown. Here we explore the effects and mechanism of RvD1 on the disruption of tight junction protein that results in the permeability edema in a model of lipopolysaccharide (LPS)-induced ALI. The severity of pulmonary edema was assessed by wet-to-dry rate and Evans blue infiltration; expressions of tight junction (TJ) proteins occludin and zona occludin-1 (ZO-1) were examined by immunofluorescence staining and western blot; mRNA in lung tissue was studied by real time-PCR; the TUNEL kit was performed for the detection of apoptosis of pulmonary barrier. Twenty-four hours after LPS inhalation by mice, wet-to-dry rate and Evans blue infiltration indicated that pretreatment with RvD1 relieved the pulmonary edema and pulmonary capillary permeability. Moreover, RvD1 attenuated the LPS-induced deterioration of TJ protein ZO-1 and occludin significantly. And we found that RvD1 increased heme oxygenase-1 (HO-1) expression contributed to the protection on the deterioration of TJs. In addition, we found that RvD1 could reduce pulmonary cellular apoptosis in LPS-induced mice. In conclusion, RvD1 possesses the ability that relieves the pulmonary edema and restores pulmonary capillary permeability and reduces disruption of TJs in LPS-induced ALI of mice, at least in part, by upregulating HO-1 expression.

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Lung Overexpression of the Vascular Endothelial Growth Factor Gene Induces Pulmonary Edema

Cited by 259 publications

References 46 publications

Decreased VEGF concentration in lung tissue and vascular injury during ARDS

Decreased VEGF concentration in lung tissue and vascular injury during ARDS

The Role of Angiopoietin 2 in Hyperoxia-Inuduced Acute Lung Injury

Resolvin D1 reduces deterioration of tight junction proteins by upregulating HO-1 in LPS-induced mice

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