Abstract
Nitric oxide (NO) produced at high concentrations by the inducible NO synthase (iNOS) is an important effector molecule involved in immune regulation and defence. In in vitro experiments we could show that NO represents a signal for triggering apoptosis in 30% of thymocytes with a concomittant decrease in CD4+CD8+ cells. In addition it protects the remaining cell population from apoptosis induced by glucocorticoids comparable to the protective effect of heat shock.
NO-induced DNA-strand breaks led to increased expression of p53, as detected by PCR analysis 2h after NO donor addition.
Furthermore, in cocultures of thymocytes with NO-producing endothelial cells the rate of thymocyte apoptosis was significantly increased, and this could be completely prevented by inhibiting NO production. Addition of dexamethasone to these cocultures did not lead to a further increase in the percentage of apoptotic thymocytes, underlining the protective effect of NO on dexamethasone-induced apoptosis.
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References
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© 1996 Springer Science+Business Media New York
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Fehsel, K., Kröncke, KD., Kolb-Bachofen, V. (1996). NO as a Physiological Signal Molecule that Triggers Thymocyte Apoptosis. In: Snyder, R., et al. Biological Reactive Intermediates V. Advances in Experimental Medicine and Biology, vol 387. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-9480-9_26
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DOI: https://doi.org/10.1007/978-1-4757-9480-9_26
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