Suppression of reactive oxygen species in endothelial cells by an antagonist of growth hormone-releasing hormone.
Animals
Cattle
Cell Line, Transformed
Endothelial Cells
/ drug effects
Growth Hormone-Releasing Hormone
/ antagonists & inhibitors
Humans
Hydrogen Peroxide
/ metabolism
Mice
NIH 3T3 Cells
Pulmonary Artery
/ cytology
Reactive Oxygen Species
/ metabolism
Receptors, Neuropeptide
/ metabolism
Receptors, Pituitary Hormone-Regulating Hormone
/ metabolism
Signal Transduction
/ drug effects
blood-brain barrier
endothelial barrier function
growth hormone
reactive oxygen species
Journal
Journal of biochemical and molecular toxicology
ISSN: 1099-0461
Titre abrégé: J Biochem Mol Toxicol
Pays: United States
ID NLM: 9717231
Informations de publication
Date de publication:
Oct 2021
Oct 2021
Historique:
revised:
16
07
2021
received:
17
05
2021
accepted:
29
07
2021
pubmed:
10
8
2021
medline:
4
2
2022
entrez:
9
8
2021
Statut:
ppublish
Résumé
Growth hormone-releasing hormone (GHRH) is a hypothalamic hormone, which regulates the secretion of growth hormone (GH) from the anterior pituitary gland. The effects of GHRH extend beyond the GH-insulin-like growth factor I axis, and that neuropeptide has been involved in the potentiation of several malignancies and other inflammatory disorders. The development of GHRH antagonists (GHRHAnt) delivers an exciting possibility to counteract the pathogenesis of the GHRH-related effects in human pathophysiology, especially when considered that GHRHAnt support endothelial barrier integrity. Those GHRHAnt-mediated effects are exerted at least in part due to the suppression of major inflammatory pathways, and the modulation of major cytoskeletal components. In the present study, we measured the production of reactive oxygen species (ROS) in bovine pulmonary artery endothelial cells, human cerebral microvascular endothelial cells, and human lung microvascular endothelial cells exposed to GHRH or a commercially available GHRHAnt. Our findings reveal the antioxidative effects of GHRHAnt in all three cell lines, which express GHRH receptors. The redox status of NIH/3T3 cells, which do not produce GHRH receptors, was not significantly affected by GHRH or GHRHAnt. Hence, the application of GHRHAnt in pathologies related to increased ROS production should be further investigated.
Identifiants
pubmed: 34369038
doi: 10.1002/jbt.22879
pmc: PMC8526391
mid: NIHMS1729171
doi:
Substances chimiques
GHRH protein, human
0
Reactive Oxygen Species
0
Receptors, Neuropeptide
0
Receptors, Pituitary Hormone-Regulating Hormone
0
Growth Hormone-Releasing Hormone
9034-39-3
Hydrogen Peroxide
BBX060AN9V
somatotropin releasing hormone receptor
F8L0ODC9D7
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e22879Subventions
Organisme : NIGMS NIH HHS
ID : P20 GM103424
Pays : United States
Organisme : Louisiana Board of Regents
ID : LEQSF(2019-22)-RD-A-26
Organisme : National Institute of General Medical Sciences of the National Institutes of Health
ID : 5 P20 GM103424-15, 3 P20 GM103424-15S1
Informations de copyright
© 2021 Wiley Periodicals LLC.
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