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Endothelial NOS-dependent activation of c-Jun NH(2)- terminal kinase by oxidized low-density lipoproteinOxidized low-density lipoprotein (oxLDL) is known to activate a number of signal transduction pathways in endothelial cells. Among these are the c-Jun NH(2)-terminal kinase (JNK), also known as stress-activated protein kinase, and extracellular signal-regulated kinase (ERK). These mitogen-activated protein kinases (MAP kinase) determine cell survival in response to environmental stress. Interestingly, JNK signaling involves redox-sensitive mechanisms and is activated by reactive oxygen and nitrogen species derived from both NADPH oxidases, nitric oxide synthases (NOS), peroxides, and oxidized low-density lipoprotein (oxLDL). The role of endothelial NOS (eNOS) in the activation of JNK in response to oxLDL has not been examined. Herein, we show that on exposure of endothelial cells to oxLDL, both ERK and JNK are activated through independent signal transduction pathways. A key role of eNOS activation through a phosphatidylinositol-3-kinase-dependent mechanism leading to phosphorylation of eNOS is demonstrated for oxLDL-dependent activation of JNK. Moreover, we show that activation of ERK by oxLDL is critical in protection against the cytotoxicity of oxLDL.
Document ID
20040088651
Acquisition Source
Legacy CDMS
Document Type
Reprint (Version printed in journal)
Authors
Go, Y. M.
(University of Alabama at Birmingham Birmingham, Alabama 35294, United States)
Levonen, A. L.
Moellering, D.
Ramachandran, A.
Patel, R. P.
Jo, H.
Darley-Usmar, V. M.
Date Acquired
August 21, 2013
Publication Date
December 1, 2001
Publication Information
Publication: American journal of physiology. Heart and circulatory physiology
Volume: 281
Issue: 6
ISSN: 0363-6135
Subject Category
Life Sciences (General)
Funding Number(s)
CONTRACT_GRANT: HL-58031
CONTRACT_GRANT: HL-60905
CONTRACT_GRANT: ES
Distribution Limits
Public
Copyright
Other
Keywords
Non-NASA Center
NASA Discipline Cell Biology

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