ArticleMediators of inflammation2016
Dephosphorylation of Y685-VE-Cadherin Involved in Pulmonary Microvascular Endothelial Barrier Injury Induced by Angiotensin II.
Article in Mediators of inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 44 citations in OpenAlex.
- Review
- From acute mast cell activation to a structured immunothrombotic and autoimmune niche in chronic spontaneous urticaria.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Distinct VE-cadherin serine and tyrosine phosphorylation sites and their role for inflammation-induced vascular permeability in vivo.Cellular and molecular life sciences : CMLS · 2025Article
- Acute aortic dissection-induced acute respiratory distress syndrome: pathogenesis and clinical implications.Frontiers in cardiovascular medicine · 2025Review
- TIMP2 ameliorates blood-brain barrier disruption in traumatic brain injury by inhibiting Src-dependent VE-cadherin internalization.The Journal of clinical investigation · 2023Article
- Is the prognosis of traumatic critically ill pediatric patients predictable? : A multicenter retrospective analysis.Wiener klinische Wochenschrift · 2023Article
- The short-chain fatty acid butyrate exerts a specific effect on VE-cadherin phosphorylation and alters the integrity of aortic endothelial cells.Frontiers in cell and developmental biology · 2023Article
- Inclusion of interleukin-6 improved the performance of postoperative acute lung injury prediction for patients undergoing surgery for thoracic aortic disease.Frontiers in cardiovascular medicine · 2023Article
- SARS-CoV-2 Spike triggers barrier dysfunction and vascular leak via integrins and TGF-β signaling.Nature communications · 2022Article
- Differential expression profile of plasma exosomal microRNAs in acute type A aortic dissection with acute lung injury.Scientific reports · 2022Article
- Preoperative acute lung injury and oxygenation impairment occurred in the patients with acute aortic dissection.BMC cardiovascular disorders · 2022Review
- SARS-CoV-2 Spike triggers barrier dysfunction and vascular leak via integrins and TGF-β signaling.bioRxiv : the preprint server for biology · 2021Article
- Phospholipase D2 restores endothelial barrier function by promoting PTPN14-mediated VE-cadherin dephosphorylation.The Journal of biological chemistry · 2020Article
- Inhibition of p38 MAPK Mitigates Lung Ischemia Reperfusion Injury by Reducing Blood-Air Barrier Hyperpermeability.Frontiers in pharmacology · 2020Article
- Carnosol as a Nrf2 Activator Improves Endothelial Barrier Function Through Antioxidative Mechanisms.International journal of molecular sciences · 2019Article
- ROS Signaling in the Pathogenesis of Acute Lung Injury (ALI) and Acute Respiratory Distress Syndrome (ARDS).Advances in experimental medicine and biology · 2017Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Angiotensin II (AngII) caused pulmonary microvascular endothelial barrier injury, which induced acute aortic dissection (AAD) combined with acute lung injury (ALI). However, the exact mechanism is unclear. We investigated the role of dephosphorylation of Y685-VE-cadherin in the AngII induced pulmonary microvascular endothelial barrier injury. Mice or pulmonary microvascular endothelial cells (PMVECs) were divided into control group, AngII group, AngII+PP2 (Src kinase inhibitor) group, and PP2 group. PP2 was used to inhibit the phosphorylation of Y685-VE-cadherin. Pathological changes, infiltration of macrophages and neutrophils, and pulmonary microvascular permeability were used to determine the pulmonary microvascular endothelial barrier function. Flow cytometry was used to determine the apoptosis of PMVECs, and immunofluorescence was used to determine the skeletal arrangement. Transendothelial resistance was used to detect the permeability of endothelial barrier. Phosphorylation of Y685-VE-cadherin was significantly reduced after AngII stimulation (
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