Document Detail


Effect of CRH on NO bioavailability, ROS production and antioxidant defense systems in endothelial EAhy926 cells.
MedLine Citation:
PMID:  20528575     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Local or 'Immune' Corticotropin-Releasing Hormone (CRH) is secreted in peripheral tissues and plays a direct immunomodulatory role as an endocrine or paracrine mediator of inflammation. The present study was undertaken to determine whether CRH affects the endothelial redox state. Accordingly, intracellular reactive oxygen species (ROS) content and peroxynitrite levels, endothelial nitric oxide synthase (eNOS) activity and nitric oxide (NO) levels as well as catalase activity, superoxide dismutase (SOD) activity and glutathione (GSH) levels were measured in the presence or absence of selective CRH receptor-1 and CRH receptor-2 inhibitors in endothelial EAhy926 cells exposed in vitro in 10(-7) M CRH for 2 h. CRH acting through both receptors induced a significant increase of ROS content (p < 0.001), catalase activity (p < 0.001) and SOD activity (p < 0.001), accompanied by a simultaneous significant decrease of eNOS activity and NO levels (p < 0.001), as well as a significant increase in nitrotyrosine (peroxynitrite) levels (p < 0.05). The data indicate that CRH may act as a regulator of pro-inflammatory mechanisms inducing adaptation of endothelial cell function to local stress.
Authors:
Sofia Gougoura; Panagiotis Liakos; George N Koukoulis
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Free radical research     Volume:  44     ISSN:  1029-2470     ISO Abbreviation:  Free Radic. Res.     Publication Date:  2010 Jul 
Date Detail:
Created Date:  2010-06-10     Completed Date:  2010-10-12     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9423872     Medline TA:  Free Radic Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  803-12     Citation Subset:  IM    
Affiliation:
Department of Endocrinology and Metabolic Diseases, Larissa University Hospital, Greece.
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MeSH Terms
Descriptor/Qualifier:
Antioxidants / metabolism*
Catalase / metabolism
Cell Line / drug effects,  metabolism
Corticotropin-Releasing Hormone / pharmacokinetics*
Culture Media, Conditioned / chemistry
Endothelial Cells / drug effects*,  metabolism
Glutathione / analysis
Humans
Nitrates / analysis
Nitric Oxide / metabolism*
Nitric Oxide Synthase Type III / metabolism
Nitrites / analysis
Peptide Fragments / pharmacology
Peptides, Cyclic / pharmacology
Pyrimidines / pharmacology
Pyrroles / pharmacology
Reactive Oxygen Species / metabolism*
Receptors, Corticotropin-Releasing Hormone / antagonists & inhibitors,  physiology
Superoxide Dismutase / metabolism
Tyrosine / analogs & derivatives,  analysis
Chemical
Reg. No./Substance:
0/Antioxidants; 0/CRF receptor type 1; 0/CRF receptor type 2; 0/Culture Media, Conditioned; 0/Nitrates; 0/Nitrites; 0/Peptide Fragments; 0/Peptides, Cyclic; 0/Pyrimidines; 0/Pyrroles; 0/Reactive Oxygen Species; 0/Receptors, Corticotropin-Releasing Hormone; 0/antalarmin; 0/astressin-2B; 10102-43-9/Nitric Oxide; 3604-79-3/3-nitrotyrosine; 55520-40-6/Tyrosine; 70-18-8/Glutathione; 9015-71-8/Corticotropin-Releasing Hormone; EC 1.11.1.6/Catalase; EC 1.14.13.39/NOS3 protein, human; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 1.15.1.1/Superoxide Dismutase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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