NDLI: The role of eNOS, iNOS, and NF-kappaB in upregulation and activation of cyclooxygenase-2 and infarct size reduction by atorvastatin.

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The role of eNOS, iNOS, and NF-kappaB in upregulation and activation of cyclooxygenase-2 and infarct size reduction by atorvastatin.

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The role of eNOS, iNOS, and NF-kappaB in upregulation and activation of cyclooxygenase-2 and infarct size reduction by atorvastatin.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Ye, Yumei Martinez, Juan D. Perez-Polo, Regino J. Lin, Yu Uretsky, Barry F. Birnbaum, Yochai
Description	Country affiliation: United States Author Affiliation: Ye Y ( Department of Internal Medicine, Univ. of Texas Medical Branch, Galveston, TX 77555-0553, USA.)
Abstract	Pretreatment with atorvastatin (ATV) reduces infarct size (IS) and increases myocardial expression of phosphorylated endothelial nitric oxide synthase (p-eNOS), inducible NOS (iNOS), and cyclooxygenase-2 (COX2) in the rat. Inhibiting COX2 abolished the ATV-induced IS limitation without affecting p-eNOS and iNOS expression. We investigated 1) whether 3-day ATV pretreatment limits IS in eNOS(-/-) and iNOS(-/-) mice and 2) whether COX2 expression and/or activation by ATV is eNOS, iNOS, and/or NF-kappaB dependent. Male C57BL/6 wild-type (WT), University of North Carolina eNOS(-/-) and iNOS(-/-) mice received ATV (10 mg.kg(-1).day(-1); ATV(+)) or water alone (ATV(-)) for 3 days. Mice underwent 30 min of coronary artery occlusion and 4 h of reperfusion, or hearts were harvested and subjected to ELISA, immunoblotting, biotin switch, and electrophoretic mobility shift assay. As a result, ATV reduced IS only in the WT mice. ATV increased eNOS, p-eNOS, iNOS, and COX2 levels and activated NF-kappaB in WT mice. It also increased myocardial COX2 activity. In eNOS(-/-) mice, ATV increased COX2 expression but not COX2 activity or iNOS expression. NF-kappaB was not activated by ATV in the eNOS(-/-) mice. In the iNOS(-/-) mice, eNOS and p-eNOS levels were increased but not iNOS and COX2 levels; however, NF-kappaB was activated. In conclusion, both eNOS and iNOS are essential for the IS-limiting effect of ATV. The expression of COX2 by ATV is iNOS, but not eNOS or NF-kappaB, dependent. Activation of COX2 is dependent on iNOS.
File Format	HTM / HTML
ISSN	03636135
e-ISSN	15221539
Journal	AJP: Heart and Circulatory Physiology
Issue Number	1
Volume Number	295
Language	English
Publisher	American Physiological Society
Publisher Date	2008-07-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Physiology Discipline Cardiology Cyclooxygenase 2 Metabolism Heptanoic Acids Pharmacology Hydroxymethylglutaryl-coa Reductase Inhibitors Myocardial Infarction Prevention & Control Myocardium Enzymology Nf-kappa B Nitric Oxide Synthase Type Ii Pyrroles 6-ketoprostaglandin F1 Alpha Animals Atorvastatin Calcium Disease Models, Animal Electrophoretic Mobility Shift Assay Enzyme Activation Enzyme-linked Immunosorbent Assay Immunoblotting Janus Kinases Antagonists & Inhibitors Mice Mice, Inbred C57bl Mice, Knockout Pathology Genetics Nitric Oxide Synthase Type Iii Peptides Phosphorylation Protein Kinase Inhibitors Time Factors Tyrphostins Up-regulation Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Cardiology and Cardiovascular Medicine

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