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

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 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 Platelet Extracellular Vesicles mediate Transfusion-related Acute Lung Injury by imbalancing the Sphingolipid Rheostat

Blood ◽  
2020 ◽  
Author(s):  
Mark J McVey ◽  
Sarah Weidenfeld ◽  
Mazharul Maishan ◽  
Chris Spring ◽  
Michael Kim ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Extracellular Vesicles ◽  
Endothelial Barrier ◽  
Barrier Dysfunction ◽  
Platelet Storage ◽  
Barrier Failure ◽  
Long Chain

Transfusion-related acute lung injury (TRALI) is a hazardous transfusion complication with an associated mortality of 5-15%. We previously showed that stored (5 days; D5) but not fresh platelets (1 day; D1) cause TRALI via ceramide mediated endothelial barrier dysfunction. As biological ceramides are hydrophobic, extracellular vesicles (EVs) may be required to shuttle these sphingolipids from platelets to endothelial cells. Adding to complexity, EV formation in turn requires ceramide. We hypothesized that ceramide-dependent EV formation from stored platelets and EV-dependent sphingolipid shuttling induce TRALI. EVs formed during storage of murine platelets were enumerated, characterized for sphingolipids and applied in a murine TRALI model in vivo and for endothelial barrier assessment in vitro. D5-EVs were more abundant, had higher long chain ceramide (C16:0, C18:0, C20:0) and lower S1P content than D1-EVs. Transfusion of D5- but not D1-EVs induced characteristic signs of lung injury in vivo and endothelial barrier disruption in vitro. Inhibition or supplementation of ceramide-forming sphingomyelinase reduced or enhanced the formation of EVs, respectively, but did not alter the injuriousness per individual EV. Barrier failure was attenuated when EVs were abundant in or supplemented with S1P. Stored human platelet D4-EVs were more numerous compared with D2-EVs, contained more long chain ceramide and less S1P, and caused more EC barrier leak. Hence, platelet-derived EVs become more numerous and more injurious (more long chain ceramide, less S1P) during storage. Blockade of sphingomyelinase, EV elimination, or supplementation of S1P during platelet storage may present promising strategies for TRALI prevention.

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