Aminophylline modulates the permeability of endothelial cells via the Slit2-Robo4 pathway in lipopolysaccharide-induced inflammation.
HUVECs
Slit2-Robo4 pathway
VE-cadherin
aminophylline
endothelial cell permeability
sepsis
Journal
Experimental and therapeutic medicine
ISSN: 1792-1015
Titre abrégé: Exp Ther Med
Pays: Greece
ID NLM: 101531947
Informations de publication
Date de publication:
Sep 2021
Sep 2021
Historique:
received:
28
08
2020
accepted:
30
06
2021
entrez:
10
8
2021
pubmed:
11
8
2021
medline:
11
8
2021
Statut:
ppublish
Résumé
Sepsis and septic shock are the main cause of mortality in intensive care units. The prevention and treatment of sepsis remains a significant challenge worldwide. The endothelial cell barrier plays a critical role in the development of sepsis. Aminophylline, a non-selective phosphodiesterase inhibitor, has been demonstrated to reduce endothelial cell permeability. However, little is known regarding the role of aminophylline in regulating vascular permeability during sepsis, as well as the potential underlying mechanisms. In the present study, the Slit2/Robo4 signaling pathway, the downstream protein, vascular endothelial (VE)-cadherin and endothelial cell permeability were investigated in a lipopolysaccharide (LPS)-induced inflammation model. It was indicated that, in human umbilical vein endothelial cells (HUVECs), LPS downregulated Slit2, Robo4 and VE-cadherin protein expression levels and, as expected, increased endothelial cell permeability
Identifiants
pubmed: 34373728
doi: 10.3892/etm.2021.10474
pii: ETM-0-0-10474
pmc: PMC8343459
doi:
Types de publication
Journal Article
Langues
eng
Pagination
1042Informations de copyright
Copyright: © Chen et al.
Déclaration de conflit d'intérêts
The authors declare that they have no competing interests.
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