Osmostress-induced apoptosis in Xenopus oocytes: Role of stress protein kinases, calpains and Smac/DIABLO

Nabil Ben Messaoud, Jicheng Yue, Daniel Valent, Ilina Katzarova, José M. López

Research output: Contribution to journalArticleResearchpeer-review

13 Citations (Scopus)

Abstract

© 2015 Messaoud et al. Hyperosmotic shock induces cytochrome c release and capase-3 activation in Xenopus oocytes, but the regulators and signaling pathways involved are not well characterized. Here we show that hyperosmotic shock induces rapid calpain activation and high levels of Smac/DIABLO release from the mitochondria before significant amounts of cytochrome c are released to promote caspase-3 activation. Calpain inhibitors or EGTA microinjection delays osmostress-induced apoptosis, and blockage of Smac/DIABLO with antibodies markedly reduces cytochrome c release and caspase-3 activation. Hyperosmotic shock also activates the p38 and JNK signaling pathways very quickly. Simultaneous inhibition of both p38 and JNK pathways reduces osmostress-induced apoptosis, while sustained activation of these kinases accelerates the release of cytochrome c and caspase-3 activation. Therefore, at least four different pathways early induced by osmostress converge on the mitochondria to trigger apoptosis. Deciphering the mechanisms of hyperosmotic shock-induced apoptosis gives insight for potential treatments of human diseases that are caused by perturbations in fluid osmolarity.
Original languageEnglish
Article numbere0124482
JournalPLoS ONE
Volume10
DOIs
Publication statusPublished - 13 Apr 2015

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