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1 Department of Pathology, 3 Department of Anesthesiology, 2 Center for Free Radical Biology, University of Alabama at Birmingham, Birmingham, Alabama 35294
The c-Jun
NH2-terminal kinase (JNK), also
known as stress-activated protein kinase, is a mitogen-activated
protein kinase that determines cell survival in response to
environmental stress. Activation of JNK involves redox-sensitive
mechanisms and physiological stimuli such as shear stress, the dragging
force generated by blood flow over the endothelium. Laminar shear
stress has antiatherogenic properties and controls structure and
function of endothelial cells by mechanisms including production of
nitric oxide (NO) and superoxide (O
2).
Here we show that both NO and O2 are
required for activation of JNK by shear stress in endothelial cells.
The present study also demonstrates that exposure of endothelial cells
to shear stress increases tyrosine nitration, a marker of reactive
nitrogen species formation. Furthermore, inhibitors or scavengers of
NO, O2, or reactive nitrogen species
prevented shear-dependent increase in tyrosine nitration and activation
of JNK. Peroxynitrite alone, added to cells as a bolus or generated
over 60 min by 3-morpholinosydnonimine, also activates JNK. These
results suggest that reactive nitrogen species, in this case most
likely peroxynitrite, act as signaling molecules in the
mechanoactivation of JNK.
nitric oxide synthase; NAD(P)H oxidase; superoxide dismutase; manganese(III)tetrakis (4-benzoic acid) porphyrin
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