PLD2 deficiency alleviates endothelial glycocalyx degradation in LPS-induced ARDS/ALI.

Autor: Kong G; Department of Intensive Care Unit, Binzhou Medical University Hospital, Binzhou, 256603, Shandong Province, China., Li D; Department of Intensive Care Unit, Yantai Yuhuangding Hospital of Qingdao University Medical College, Yantai, 264000, Shandong Province, China., Liu X; Department of Cell Biology, Binzhou Medical University, Yantai, 264003, Shandong Province, China. Electronic address: liuxy@bzmc.edu.cn., Feng J; Department of Pulmonary and Critical Care Medicine, Yantaishan Hospital, Yantai, 264000, Shandong Province, China., Ning F; Department of Intensive Care Unit, Binzhou Medical University Hospital, Binzhou, 256603, Shandong Province, China., Huang X; Department of Intensive Care Unit, Binzhou Medical University Hospital, Binzhou, 256603, Shandong Province, China., Qi B; Department of Cardiovascular Surgery Intensive Care Unit, Yantai Yuhuangding Hospital of Qingdao University Medical College, Yantai, 264000, Shandong Province, China., Qu J; Department of Critical Care Medicine, Yantaishan Hospital, Yantai, 264000, Shandong Province, China., Wang X; Department of Intensive Care Unit, Binzhou Medical University Hospital, Binzhou, 256603, Shandong Province, China. Electronic address: hxicuwxz@163.com.
Jazyk: angličtina
Zdroj: Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2024 Jul 05; Vol. 716, pp. 150019. Date of Electronic Publication: 2024 Apr 26.
DOI: 10.1016/j.bbrc.2024.150019
Abstrakt: - Acute respiratory distress syndrome (ARDS)/acute lung injury (ALI) is a life-threatening condition marked by severe lung inflammation and increased lung endothelial barrier permeability. Endothelial glycocalyx deterioration is the primary factor of vascular permeability changes in ARDS/ALI. Although previous studies have shown that phospholipase D2 (PLD2) is closely related to the onset and progression of ARDS/ALI, its role and mechanism in the damage of endothelial cell glycocalyx remains unclear. We used LPS-induced ARDS/ALI mice (in vivo) and LPS-stimulated injury models of EA.hy926 endothelial cells (in vitro). We employed C57BL/6 mice, including wild-type and PLD2 knockout (PLD2 -/- ) mice, to establish the ARDS/ALI model. We applied immunofluorescence and ELISA to examine changes in syndecan-1 (SDC-1), matrix metalloproteinase-9 (MMP9), inflammatory cytokines (TNF-α, IL-6, and IL-1β) levels and the effect of external factors, such as phosphatidic acid (PA), 1-butanol (a PLD inhibitor), on SDC-1 and MMP9 expression levels. We found that PLD2 deficiency inhibits SDC-1 degradation and MMP9 expression in LPS-induced ARDS/ALI. Externally added PA decreases SDC-1 levels and increases MMP9 in endothelial cells, hence underlining PA's role in SDC-1 degradation. Additionally, PLD2 deficiency decreases the production of inflammatory cytokines (TNF-α, IL-6, and IL-1β) in LPS-induced ARDS/ALI. In summary, these findings suggest that PLD2 deficiency plays a role in inhibiting the inflammatory process and protecting against endothelial glycocalyx injury in LPS-induced ARDS/ALI.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024. Published by Elsevier Inc.)
Databáze: MEDLINE
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