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Mechanisms of cell signaling by nitric oxide and peroxynitrite: from mitochondria to MAP kinasesMany of the biological and pathological effects of nitric oxide (NO) are mediated through cell signaling pathways that are initiated by NO reacting with metalloproteins. More recently, it has been recognized that the reaction of NO with free radicals such as superoxide and the lipid peroxyl radical also has the potential to modulate redox signaling. Although it is clear that NO can exert both cytotoxic and cytoprotective actions, the focus of this overview are those reactions that could lead to protection of the cell against oxidative stress in the vasculature. This will include the induction of antioxidant defenses such as glutathione, activation of mitogen-activated protein kinases in response to blood flow, and modulation of mitochondrial function and its impact on apoptosis. Models are presented that show the increased synthesis of glutathione in response to shear stress and inhibition of cytochrome c release from mitochondria. It appears that in the vasculature NO-dependent signaling pathways are of three types: (i) those involving NO itself, leading to modulation of mitochondrial respiration and soluble guanylate cyclase; (ii) those that involve S-nitrosation, including inhibition of caspases; and (iii) autocrine signaling that involves the intracellular formation of peroxynitrite and the activation of the mitogen-activated protein kinases. Taken together, NO plays a major role in the modulation of redox cell signaling through a number of distinct pathways in a cellular setting.
Document ID
20040112418
Acquisition Source
Legacy CDMS
Document Type
Reprint (Version printed in journal)
Authors
Levonen, A. L.
(University of Alabama at Birmingham 35294-0019, United States)
Patel, R. P.
Brookes, P.
Go, Y. M.
Jo, H.
Parthasarathy, S.
Anderson, P. G.
Darley-Usmar, V. M.
Date Acquired
August 21, 2013
Publication Date
April 1, 2001
Publication Information
Publication: Antioxidants & redox signalling
Volume: 3
Issue: 2
ISSN: 1523-0864
Subject Category
Life Sciences (General)
Funding Number(s)
CONTRACT_GRANT: ES10167
CONTRACT_GRANT: AA12613
CONTRACT_GRANT: HL58031
Distribution Limits
Public
Copyright
Other
Keywords
Non-NASA Center
Review
NASA Discipline Cell Biology
Review, Academic

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