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PLoS One 2015 Apr 13;104:e0124482. doi: 10.1371/journal.pone.0124482.
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Osmostress-induced apoptosis in Xenopus oocytes: role of stress protein kinases, calpains and Smac/DIABLO.

Ben Messaoud N , Yue J , Valent D , Katzarova I , López JM .

Hyperosmotic shock induces cytochrome c release and caspase-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.

PubMed ID: 25866890
PMC ID: PMC4395108
Article link: PLoS One

Species referenced: Xenopus laevis
Genes referenced: actl6a casp3.2 diablo grap2 map2k6 map3k1 mapk14 mapk8 myc prkaa1

Disease Ontology terms: diabetic cataract [+]

Article Images: [+] show captions
References [+] :
Adrain, Apoptosis-associated release of Smac/DIABLO from mitochondria requires active caspases and is blocked by Bcl-2. 2001, Pubmed