Vascular Endothelial Growth Factor in Acute Lung Injury and Acute Respiratory Distress Syndrome

Barratt, Shaney; Medford, Andrew R L; Millar, Ann

doi:10.1159/000356034

Cited by 71 publications

(63 citation statements)

References 129 publications

(182 reference statements)

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“…There are alterations in the plasma levels of VEGF, with associated falls in intrapulmonary levels seen in the early, exudative phase of lung injury; these changes normalise in recovery [34]. The observation that alveolar levels of VEGF are twice the level shown to induce angiogenesis [35], with restriction of these processes in healthy lung [36], leads to paradoxical and opposing views of the role of VEGF in normal and diseased lung [37,38]. It has been suggested that regulation of the biological activity of VEGF could provide an explanation of previous observations.…”

Section: Pathogenesis Of Ardsmentioning

confidence: 99%

Advances in Understanding of the Pathogenesis of Acute Respiratory Distress Syndrome

2015

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The clinical syndrome of acute lung injury (ALI) occurs as a result of an initial acute systemic inflammatory response. This can be consequent to a plethora of insults, either direct to the lung or indirect. The insult results in increased epithelial permeability, leading to alveolar flooding with a protein-rich oedema fluid. The resulting loss of gas exchange leads to acute respiratory failure and typically catastrophic illness, termed acute respiratory distress syndrome (ARDS), requiring ventilatory and critical care support. There remains a significant disease burden, with some estimates showing 200,000 cases each year in the USA with a mortality approaching 50%. In addition, there is a significant burden of morbidity in survivors. There are currently no disease-modifying therapies available, and the most effective advances in caring for these patients have been in changes to ventilator strategy as a result of the ARDS network studies nearly 15 years ago. Here, we will give an overview of more recent advances in the understanding of the cellular biology of ALI and highlight areas that may prove fertile for future disease-modifying therapies.

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Section: Pathogenesis Of Ardsmentioning

confidence: 99%

Advances in Understanding of the Pathogenesis of Acute Respiratory Distress Syndrome

2015

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“…27 Since its discovery, VEGF has been implicated in a wide range of inflammatory diseases, including pulmonary inflammation, such as ARDS, VILI, fibrosis, and asthma. [28][29][30][31][32] While VEGF plays a critical role in organogenesis, 33,34 its expression in lungs persists into adulthood and remains the predominant source of VEGF in adults. 35,36 Given the physiological role played by VEGF in lung maintenance and homeostasis, the involvement of VEGF in the pathogenesis of ARDS has been well investigated.…”

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confidence: 99%

Sp1‐Mediated Nonmuscle Myosin Light Chain Kinase Expression and Enhanced Activity in Vascular Endothelial Growth Factor–Induced Vascular Permeability

et al. 2015

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Despite the important role played by the nonmuscle isoform of myosin light chain kinase (nmMLCK) in vascular barrier regulation and the implication of both nmMLCK and vascular endothelial growth factor (VEGF) in the pathogenesis of acute respiratory distress syndrome (ARDS), the role played by nmMLCK in VEGF-induced vascular permeability is poorly understood. In this study, the role played by nmMLCK in VEGF-induced vascular hyperpermeability was investigated. Human lung endothelial cell barrier integrity in response to VEGF is examined in both the absence and the presence of nmMLCK small interfering RNAs. Levels of nmMLCK messenger RNA (mRNA), protein, and promoter activity expression were monitored after VEGF stimulation in lung endothelial cells. nmMYLK promoter activity was assessed using nmMYLK promoter luciferase reporter constructs with a series of nested deletions. nmMYLK transcriptional regulation was further characterized by examination of a key transcriptional factor. nmMLCK plays an important role in VEGFinduced permeability. We found that activation of the VEGF signaling pathway in lung endothelial cells increases MYLK gene product at both mRNA and protein levels. Increased nmMLCK mRNA and protein expression is a result of increased nmMYLK promoter activity, regulated in part by binding of the Sp1 transcription factor on triggering by the VEGF signaling pathway. Taken together, these findings suggest that MYLK is an important ARDS candidate gene and a therapeutic target that is highly influenced by excessive VEGF concentrations in the inflamed lung.

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“…AT-II, and secreting surfactant protein (Barratt et al, 2014). VEGF also has chemotaxis ability to attract alveolar macrophages, which express VEGF receptor 2 (VEGFR2) (Clauss et al, 1996;Ferrara et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Characterization of Influenza A Virus Infection in Mouse Pulmonary Stem/Progenitor Cells

Chao

Lin

et al. 2020

Front. Microbiol.

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Vascular Endothelial Growth Factor in Acute Lung Injury and Acute Respiratory Distress Syndrome

Cited by 71 publications

References 129 publications

Advances in Understanding of the Pathogenesis of Acute Respiratory Distress Syndrome

Advances in Understanding of the Pathogenesis of Acute Respiratory Distress Syndrome

Sp1‐Mediated Nonmuscle Myosin Light Chain Kinase Expression and Enhanced Activity in Vascular Endothelial Growth Factor–Induced Vascular Permeability

Characterization of Influenza A Virus Infection in Mouse Pulmonary Stem/Progenitor Cells

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