Previous in vitro studies showed that rat hypothalamic explants release interleukin-1β (IL-1β); such release is significantly increased by several stimuli including 56 mM KCl and NO-donors in 20-min experiments. Here we tested the hypothesis that the above stimuli act via a mechanism involving cleavage of the IL-1β precursor by interleukin-1β converting enzyme (ICE, also referred to as caspase-1). A cell-permeable form of the caspase-1 inhibitor I and two different stimuli, 56 mM KCl and sodium nitroprusside (SNP), were used. The inhibitor was able to counteract the increase in IL-1β release induced by both K+ and SNP, while having no effect on basal release.
Tringali, G., Dello Russo, C., Vairano, M., Preziosi, P., Navarra, P., Depolarization and a NO-donor stimulate interleukin-1b release from the rat hypothalamus via a mechanism involving caspase-1., <<NEUROSCIENCE LETTERS>>, 1999; (276 (2)): 119-122. [doi:10.1016/s0304-3940(99)00806-x] [https://hdl.handle.net/10807/344996]
Depolarization and a NO-donor stimulate interleukin-1b release from the rat hypothalamus via a mechanism involving caspase-1.
Tringali, Giuseppe;Preziosi, Paolo;Navarra, Pierluigi
1999
Abstract
Previous in vitro studies showed that rat hypothalamic explants release interleukin-1β (IL-1β); such release is significantly increased by several stimuli including 56 mM KCl and NO-donors in 20-min experiments. Here we tested the hypothesis that the above stimuli act via a mechanism involving cleavage of the IL-1β precursor by interleukin-1β converting enzyme (ICE, also referred to as caspase-1). A cell-permeable form of the caspase-1 inhibitor I and two different stimuli, 56 mM KCl and sodium nitroprusside (SNP), were used. The inhibitor was able to counteract the increase in IL-1β release induced by both K+ and SNP, while having no effect on basal release.
I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
