17
17β-estradiol
apurinic/apyrimidinic endonuclease-1/redox factor-1
calcium
endothelial cells
estrogen receptor
exosome
Journal
Biomedicines
ISSN: 2227-9059
Titre abrégé: Biomedicines
Pays: Switzerland
ID NLM: 101691304
Informations de publication
Date de publication:
18 Aug 2021
18 Aug 2021
Historique:
received:
11
06
2021
revised:
06
08
2021
accepted:
16
08
2021
entrez:
27
8
2021
pubmed:
28
8
2021
medline:
28
8
2021
Statut:
epublish
Résumé
Apurinic/apyrimidinic endonuclease-1/redox factor-1 (APE1/Ref-1) is a multifunctional protein that can be secreted, and recently suggested as new biomarker for vascular inflammation. However, the endogenous hormones for APE1/Ref-1 secretion and its underlying mechanisms are not defined. Here, the effect of twelve endogenous hormones on APE1/Ref-1 secretion was screened in cultured vascular endothelial cells. The endogenous hormones that significantly increased APE1/Ref-1 secretion was 17β-estradiol (E2), 5?-dihydrotestosterone, progesterone, insulin, and insulin-like growth factor. The most potent hormone inducing APE1/Ref-1 secretion was E2, which in cultured endothelial cells, E2 for 24 h increased APE1/Ref-1 secretion level of 4.56 ± 1.16 ng/mL, compared to a basal secretion level of 0.09 ± 0.02 ng/mL. Among the estrogens, only E2 increased APE1/Ref-1 secretion, not estrone and estriol. Blood APE1/Ref-1 concentrations decreased in ovariectomized (OVX) mice but were significantly increased by the replacement of E2 (0.39 ± 0.09 ng/mL for OVX vs. 4.67 ± 0.53 ng/mL for OVX + E2). E2-induced APE1/Ref-1secretion was remarkably suppressed by the estrogen receptor (ER) blocker fulvestrant and intracellular Ca
Identifiants
pubmed: 34440244
pii: biomedicines9081040
doi: 10.3390/biomedicines9081040
pmc: PMC8394342
pii:
doi:
Types de publication
Journal Article
Langues
eng
Subventions
Organisme : National Research Foundation of Korea
ID : 2014R1A6A1029617
Organisme : National Research Foundation of Korea
ID : 2020R1I1A1A01072327
Organisme : Ministry of Science, ICT and Future Planning
ID : 2020R1C1C1014490
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