I am so curious about the diverse roles of NO. While discussing the stimulated production of NO by cytokines in osteoarthritis, the B. Dozin et al in the article, Response of young, aged and osteoarthritic human articular chondrocytes to inflammatory cytokines, mentioned NO as a signaling molecule. NO acts on Gproteins activating the second messenger cyclic GMP to stimulate countlesss down stream effects. The little molecule also binds in the mitochondria matrix inhibiting oxidative phosphorylation. The general role is to kill bacteria but the host cells are often targeted too.Turns out this little radical is even qualified as a neurotransmitter. Important in developing long term memory, NO is also implemented in neuronal cell death. In addition, NO is the main signaler of vasodialation in the periphery.
My question pertains to all of the literature we have read so far in these inflammation patholgies. So often the effective treatments involve suppressing NO sythesis. How can we suppress the destructive functions of this essential molecule while maintaining the beneficial? How do we determine what role NO is playing in the tissue being studied?
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This reminds me of the same problem that cancer patients undergoing chemotherapy face, while killing rapid growing cancer cells it also kills healthy cells of hair follicles, bone marrow, etc. Figuring out how to block one pathway to cells while enhancing another pathway would be interesting.
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