Soluble RAGE attenuates AngII-induced endothelial hyperpermeability by disrupting HMGB1-mediated crosstalk between AT1R and RAGE.
Angiotensin II
/ genetics
Animals
Antigens, CD
/ genetics
Antigens, Neoplasm
/ genetics
Aorta
/ metabolism
Atherosclerosis
/ genetics
Cadherins
/ genetics
Capillary Permeability
/ genetics
Cardiovascular Diseases
/ genetics
Endothelial Cells
/ metabolism
HMGB1 Protein
/ genetics
Human Umbilical Vein Endothelial Cells
/ metabolism
Humans
Hypertension
/ genetics
Inflammation
/ genetics
Ligands
Mice
Mice, Knockout
Mitogen-Activated Protein Kinases
/ genetics
RNA, Small Interfering
/ genetics
Receptor, Angiotensin, Type 1
/ genetics
Signal Transduction
/ genetics
Journal
Experimental & molecular medicine
ISSN: 2092-6413
Titre abrégé: Exp Mol Med
Pays: United States
ID NLM: 9607880
Informations de publication
Date de publication:
27 09 2019
27 09 2019
Historique:
received:
19
12
2018
accepted:
08
07
2019
revised:
03
07
2019
entrez:
29
9
2019
pubmed:
29
9
2019
medline:
23
6
2020
Statut:
epublish
Résumé
Increased endothelial permeability, one of the earliest signs of endothelial dysfunction, is associated with the development of cardiovascular diseases such as hypertension and atherosclerosis. Recent studies suggest that the receptor for advanced glycation end products (RAGE) regulates endothelial permeability in inflammation. In the present study, we investigated the regulatory mechanism of RAGE in endothelial hyperpermeability induced by angiotensin II (Ang II), a well-known inflammatory mediator, and the potential therapeutic effect of soluble RAGE (sRAGE), a decoy receptor for RAGE ligands. For in vitro studies, Ang II-treated human umbilical vein endothelial cells (HUVECs) were treated with siRNA specific to either RAGE or sRAGE to disrupt RAGE-mediated signaling. Endothelial permeability was estimated using FITC-labeled dextran 40 and a resistance meter. To evaluate intercellular junction disruption, VE-cadherin expression was examined by western blotting and immunocytochemistry. Ang II increased the expression of the Ang II type 1 receptor (AT1R) and RAGE, and this increase was inhibited by sRAGE. sRAGE prevented Ang II-induced VE-cadherin disruption in HUVECs. For in vivo studies, Ang II-infused, atherosclerosis-prone apolipoprotein E knockout mice were utilized. Endothelial permeability was assessed by Evans blue staining of the aorta. Ang II increased endothelial barrier permeability, and this effect was significantly attenuated by sRAGE. Our data demonstrate that blockade of RAGE signaling using sRAGE attenuates Ang II-induced endothelial barrier permeability in vitro and in vivo and indicate the therapeutic potential of sRAGE in controlling vascular permeability under pathological conditions.
Identifiants
pubmed: 31562296
doi: 10.1038/s12276-019-0312-5
pii: 10.1038/s12276-019-0312-5
pmc: PMC6802637
doi:
Substances chimiques
AGTR1 protein, human
0
Antigens, CD
0
Antigens, Neoplasm
0
Cadherins
0
HMGB1 Protein
0
HMGB1 protein, human
0
Ligands
0
RNA, Small Interfering
0
Receptor, Angiotensin, Type 1
0
cadherin 5
0
Angiotensin II
11128-99-7
MOK protein, human
EC 2.7.11.22
Mitogen-Activated Protein Kinases
EC 2.7.11.24
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1-15Subventions
Organisme : National Research Foundation of Korea (NRF)
ID : 2018R1A1A1A05078230
Pays : International
Organisme : National Research Foundation of Korea (NRF)
ID : 2016R1C1B2016115
Pays : International
Organisme : National Research Foundation of Korea (NRF)
ID : 2015R1A2A2A01007346
Pays : International
Organisme : Ministry of Health and Welfare (Ministry of Health, Welfare and Family Affairs)
ID : HI08C2149
Pays : International
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