ArticlePloS one2015
Osmostress-induced apoptosis in Xenopus oocytes: role of stress protein kinases, calpains and Smac/DIABLO.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- p38α and p38β regulate osmostress-induced apoptosis.The Journal of biological chemistry · 2025Article
- SMAC Mimetics for the Treatment of Lung Carcinoma: Present Development and Future Prospects.Mini reviews in medicinal chemistry · 2024Review
- Article
- Exogenous Melatonin Ameliorates the Negative Effect of Osmotic Stress in Human and Bovine Ovarian Stromal Cells.Antioxidants (Basel, Switzerland) · 2022Article
- In vitro cell cycle oscillations exhibit a robust and hysteretic response to changes in cytoplasmic density.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- GABA Receptor Agonists Protect From Excitotoxic Damage Induced by AMPA in Oligodendrocytes.Frontiers in pharmacology · 2022Article
- Effects of Ferrocenyl 4-(Imino)-1,4-Dihydro-quinolines onInternational journal of molecular sciences · 2020Article
- Understanding MAPK Signaling Pathways in Apoptosis.International journal of molecular sciences · 2020Review
- Bicalutamide enhances fodrin-mediated apoptosis through calpain in LNCaP.Experimental biology and medicine (Maywood, N.J.) · 2018Article
- Melittin induces human gastric cancer cell apoptosis via activation of mitochondrial pathway.World journal of gastroenterology · 2016Article
- Article
- Hyperosmotic Shock Engages Two Positive Feedback Loops through Caspase-3-dependent Proteolysis of JNK1-2 and Bid.The Journal of biological chemistry · 2015Article
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- Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.