ArticleAmerican journal of respiratory cell and molecular biology2008
Platelets enhance endothelial adhesiveness in high tidal volume ventilation.
Article in American journal of respiratory cell and molecular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Ventilator-Induced Lung Injury: Mechanotransduction and Potential Therapeutic Targets.MedComm · 2026Review
- Arterial Thrombosis in Acute Respiratory Infections: An Underestimated but Clinically Relevant Problem.Journal of clinical medicine · 2024Review
- Characterization of Platelet Biologic Markers in the Early Pathogenesis of Postoperative Acute Respiratory Distress Syndrome.Critical care explorations · 2022Article
- The Role of Von Willebrand Factor in the Pathogenesis of Pulmonary Vascular Thrombosis in COVID-19.Viruses · 2022Article
- Endothelial cells, neutrophils and platelets: getting to the bottom of an inflammatory triangle.Open biology · 2020Review
- Pulmonary Artery Thrombosis: A Diagnosis That Strives for Its Independence.International journal of molecular sciences · 2020Review
- Amicus or Adversary Revisited: Platelets in Acute Lung Injury and Acute Respiratory Distress Syndrome.American journal of respiratory cell and molecular biology · 2018Review
- Platelets and Multi-Organ Failure in Sepsis.International journal of molecular sciences · 2017Review
- Platelets in Pulmonary Immune Responses and Inflammatory Lung Diseases.Physiological reviews · 2016Review
- Platelets in the pathogenesis of acute respiratory distress syndrome.American journal of physiology. Lung cellular and molecular physiology · 2015Review
- Emerging therapies for the prevention of acute respiratory distress syndrome.Therapeutic advances in respiratory disease · 2015Review
- Platelets in lung biology.Annual review of physiology · 2013Review
- Erythrocytes induce proinflammatory endothelial activation in hypoxia.American journal of respiratory cell and molecular biology · 2013Article
- Platelets induce endothelial tissue factor expression in a mouse model of acid-induced lung injury.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- Article
- Statins STAT for (over)ventilated patients?Critical care (London, England) · 2010Review
- Soluble p-selectin and the risk of primary graft dysfunction after lung transplantation.Chest · 2009Article
- Crosstalk signaling between alveoli and capillaries.Pulmonary circulationArticle
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Although platelets induce lung inflammation, leading to acute lung injury (ALI), the extent of platelet-endothelial cell (EC) interactions remains poorly understood. Here, in a ventilation-stress model of lung inflammation, we show that platelet-EC interactions are important. We obtained freshly isolated lung endothelial cells (FLECs) from isolated, blood-perfused rat lungs exposed to ventilation at low tidal volume (LV) or stress-inducing high tidal volume (HV). Immunofluorescence and immunoprecipitation studies revealed HV-induced increases in cell-surface von Willebrand factor (vWf) expression on FLEC. This increased expression was inhibited by platelet removal from the lung perfusion and by including a P-selectin-blocking antibody in the lung perfusion. The expression was also blocked in lungs from P-selectin knockout (P sel(-/-)) mice perfused with autologous blood, but not with heterologous wild-type blood containing P-selectin-expressing platelets. These findings indicate that in ventilation stress, platelets transfer vWf to the EC surface and that platelet P-selectin plays a critical role in this transfer. Further evidence for such intercellular transfers was the HV-induced FLEC expressions of platelet glycoprotein 1b and of platelet P-selectin. We conclude that in ventilation stress, platelets deposit leukocyte- and platelet-binding proteins on the EC surface, thereby establishing the proinflammatory phenotype of the vascular lining.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.