Dephosphorylation of Y685-VE-Cadherin Involved in Pulmonary Microvascular Endothelial Barrier Injury Induced by Angiotensin II

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 pulmona...

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Bibliographic Details
Published in:Mediators of inflammation 2016-01, Vol.2016 (2016), p.1-10
Main Authors: Li, Bowen, Ren, Wei, Liu, Huagang, Dai, Feifeng, Wang, Zhiwei, Wu, Zhiyong, Chang, Jinxing
Format: Article
Language:English
Subjects:
Adult
Aged
Angiotensin
Angiotensin II - metabolism
Animals
Antigens, CD - genetics
Antigens, CD - metabolism
Apoptosis
Cadherins
Cadherins - genetics
Cadherins - metabolism
Capillary Permeability
Case-Control Studies
Endothelium, Vascular - metabolism
Female
Health aspects
Humans
Laboratory animals
Lung - blood supply
Lung diseases
Male
Mice
Mice, Inbred C57BL
Microcirculation
Middle Aged
Morphology
Mutation
Observations
Permeability
Phosphorylation
Physiological aspects
Rats
Rodents
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Summary: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 (P
ISSN:0962-9351
1466-1861
DOI:10.1155/2016/8696481