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G protein-coupled estrogen receptor-1 is involved in the protective effect of protocatechuic aldehyde against endothelial dysfunction.

 Byung Soo Kong  ;  Yoon Hee Cho  ;  Eun Jig Lee 
 PLOS ONE, Vol.9(11) : e113242, 2014 
Journal Title
Issue Date
Animals ; Aorta, Thoracic/drug effects* ; Aorta, Thoracic/metabolism ; Benzaldehydes/pharmacology* ; Benzodioxoles/pharmacology ; Carotid Artery Injuries/drug therapy* ; Carotid Artery Injuries/metabolism ; Carotid Artery Injuries/pathology ; Catechols/pharmacology* ; Cyclic AMP/metabolism ; Disease Models, Animal ; Human Umbilical Vein Endothelial Cells ; Hydrogen Peroxide/pharmacology ; Male ; Neointima/drug therapy* ; Neointima/etiology ; Organ Culture Techniques/methods ; Quinolines/pharmacology ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species/metabolism ; Receptors, Estrogen ; Receptors, G-Protein-Coupled/metabolism*
Protocatechuic aldehyde (PCA), a phenolic aldehyde, has therapeutic potency against atherosclerosis. Although PCA is known to inhibit the migration and proliferation of vascular smooth muscle cells and intravascular thrombosis, the underlying mechanism remains unclear. In this study, we investigated the protective effect of PCA on endothelial cells and injured vessels in vivo in association with G protein-coupled estrogen receptor-1 (GPER-1). With PCA treatment, cAMP production was increased in HUVECs, while GPER-1 expression was increased in both HUVECs and a rat aortic explant. PCA and G1, a GPER-1 agonist, reduced H2O2 stimulated ROS production in HUVECs, whereas, G15, a GPER-1 antagonist, increased ROS production further. These elevations were inhibited by co-treatment with PCA or G1. TNFα stimulated the expression of inflammatory markers (VCAM-1, ICAM-1 and CD40), phospho-NF-κB, phospho-p38 and HIF-1α; however, co-treatment with PCA or G1 down-regulated this expression significantly. Likewise, increased expression of inflammatory markers by treatment with G15 was inhibited by co-treatment with PCA. In re-endothelization, aortic ring sprouting and neointima formation assay, rat aortas treated with PCA or G1 showed accelerated re-endothelization of the endothelium and reduced sprouting and neointima formation. However, aortas from G15-treated rats showed decelerated re-endothelization and increased sprouting and neointima formation. The effects of G15 were restored by co-treatment with PCA or G1. Also, in the endothelia of these aortas, PCA and G1 increased CD31 and GPER-1 and decreased VCAM-1 and CD40 expression. In contrast, the opposite effect was observed in G15-treated endothelium. These results suggest that GPER-1 might mediate the protective effect of PCA on the endothelium.
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1. College of Medicine (의과대학) > Research Institute (부설연구소) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
Yonsei Authors
Kong, Byung Soo(공병수)
Lee, Eun Jig(이은직) ORCID logo https://orcid.org/0000-0002-9876-8370
Cho, Yoon Hee(조윤희)
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