scholarly journals ASK1-p38 cascaded signal mediates pulmonary microvascular endothelial barrier injury induced by the return of PHSML in rats

RSC Advances ◽  
2019 ◽  
Vol 9 (9) ◽  
pp. 4870-4875
Author(s):  
Muhammad Fawad ◽  
Muhammad Abbas ◽  
Limin Zhang ◽  
Yuping Zhang ◽  
Yaxiong Guo
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Hemorrhagic Shock ◽  
Endothelial Barrier ◽  
Vascular Endothelial ◽  
Barrier Dysfunction ◽  
Endothelial Barrier Dysfunction ◽  
Mesenteric Lymph ◽  
Microvascular Endothelial

The return of post-hemorrhagic shock mesenteric lymph (PHSML) induces pulmonary vascular endothelial barrier dysfunction, which results in acute lung injury.

scholarly journals Alda-1 Protects Against Acrolein-Induced Acute Lung Injury and Endothelial Barrier Dysfunction

2017 ◽  
Vol 57 (6) ◽  
pp. 662-673 ◽  
Author(s):  
Qing Lu ◽  
Miles Mundy ◽  
Eboni Chambers ◽  
Thilo Lange ◽  
Julie Newton ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Endothelial Barrier ◽  
Barrier Dysfunction ◽  
Endothelial Barrier Dysfunction

scholarly journals Roles of VE-Cadherin in Hypoxia Induced Injury of Pulmonary Microvascular Endothelial Barrier

2021 ◽  
Vol 24 (4) ◽  
pp. E764-E768
Author(s):  
Lizhe Zhong ◽  
Xiurong Gao ◽  
Yongli Chen ◽  
Zhaoxiang Yu ◽  
Shuo Jin ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Acute Lung Injury ◽  
Endothelial Barrier ◽  
Microvascular Endothelial Cells ◽  
Barrier Dysfunction ◽  
Barrier Methods ◽  
Endothelial Barrier Dysfunction ◽  
Microvascular Endothelial ◽  
Induced Apoptosis

Background: Hypoxia induced injury of pulmonary microvascular endothelial barrier is closely related to the pathogenesis of acute lung injury after lung transplantation. VE-cadherin is an important structural molecule for pulmonary microvascular endothelial barrier. In this study, we aim to investigate the roles of VE-cadherin in hypoxia induced injury of pulmonary microvascular endothelial barrier. Methods: Rat model of hypoxia and cultured pulmonary microvascular endothelial cells (PMVECs) were utilized. Determination of PMVECs apoptosis, skeleton combination was conducted to verify the effects of hypoxia on injury of pulmonary microvascular endothelial barrier. In addition, VE-cadherin expression was modulated by administration of siRNA in order to investigate the roles of VE-cadherin in hypoxia induced PMVECs apoptosis and skeleton recombination. Results: Our data indicated that expression of VE-cadherin was down-regulated in hypoxia-exposed PMVECs. Whereas, in the cells treated using siRNA, down-regulation of VE-cadherin did not trigger PMVECs apoptosis, but it increased the sensitivity of PMVECs to the hypoxia induced apoptosis. In cases of hypoxia, the expression of VE-cadherin was significantly down-regulated, together with endothelial skeleton recombination and increase of permeability, which then triggered endothelial barrier dysfunction. Conclusions: These data verify that VE-cadherin expression played an important role in hypoxia induced PMVECs apoptosis and cellular skeletal recombination.

Cardamonin protects septic mice from acute lung injury by preventing endothelial barrier dysfunction

2012 ◽  
Vol 26 (7) ◽  
pp. 282-290 ◽  
Author(s):  
Zhifeng Wei ◽  
Jian Yang ◽  
Yu-Feng Xia ◽  
Wen-Zhe Huang ◽  
Zheng-Tao Wang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Endothelial Barrier ◽  
Barrier Dysfunction ◽  
Endothelial Barrier Dysfunction

scholarly journals mTORC2 Activation Mediated by Mesenchymal Stem Cell-Secreted Hepatocyte Growth Factors for the Recovery of Lipopolysaccharide-Induced Vascular Endothelial Barrier

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Shan-Shan Meng ◽  
Feng-Mei Guo ◽  
Li-Li Huang ◽  
Ying-Zi Huang ◽  
Jian-Feng Xie ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Endothelial Barrier ◽  
Vascular Endothelial ◽  
Protective Effects ◽  
Barrier Dysfunction ◽  
Endothelial Barrier Dysfunction ◽  
Microvascular Endothelial ◽  
Hepatocyte Growth

Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is characterized by pulmonary microvascular endothelial barrier dysfunction. Mesenchymal stem cell-secreted hepatocyte growth factor (HGF) has positive effects of lipopolysaccharide- (LPS-) induced pulmonary endothelial barrier. Studies have exhibited the mammalian TORC1 (mTORC1) signaling is of potent angiogenesis effects. The mTOR protein kinase has two distinct multiprotein complexes mTORC1 and mTORC2 that regulate different branches of the mTOR network. However, detailed mTORC2 mechanisms of HGF protective effects remain poorly defined. Therefore, the aim of this study was to determine whether mTORC2 mediated protective effects of MSC-secreted HGF against LPS-induced pulmonary microvascular endothelial barrier dysfunction activated like mTORC1 activation. We introduced MSC-PMVEC coculture transwell system and recombinant murine HGF on LPS-induced endothelial cell barrier dysfunction in vitro and then explored potential mechanisms by lentivirus vector-mediated HGF, mTORC1 (raptor), and mTORC2 (rictor) gene knockdown modification. Endothelial paracellular and transcellular permeability, adherent junction protein (VE-Cadherin), cell proliferation, apoptosis, and mTOR-associated proteins were tested. These revealed that HGF could promote quick reestablishment of adherent junction VE-cadherin and decrease endothelial paracellular and transcellular permeability during LSP-induced endothelial dysfunction with the involvement of mTORC2 (rictor) and mTORC1 (raptor) pathways. Raptor and rictor knockdown in LPS-induced PMEVECs with stimulation of HGF increased apoptosis ratio, activated Cleaved-Caspase-3 expression, and downregulated cell proliferation. Moreover, mTORC2/Akt but not mTORC2/PKC had significance on HGF endothelial protective effects. Taken together, these highlight activation mTORC2 pathway could also contribute to vascular endothelial barrier recovery by MSC-secreted HGF in LPS stimulation.

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