ArticleThe Journal of physiology2005
Cell shrinkage as a signal to apoptosis in NIH 3T3 fibroblasts.
Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 142 citations in OpenAlex.
- p38α and p38β regulate osmostress-induced apoptosis.The Journal of biological chemistry · 2025Article
- Quantification of cellular phototoxicity of organelle stains by the dynamics of microtubule polymerization.View (Beijing, China) · 2024Article
- In-Foam Bioprinting: An Embedded Bioprinting Technique with Self-Removable Support Bath.Small science · 2024Article
- New role for the anandamide metabolite prostaglandin FJournal of lipid research · 2023Article
- Serine protease 35 regulates the fibroblast matrisome in response to hyperosmotic stress.Science advances · 2023Article
- Review
- 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
- Evidence for macromolecular crowding as a direct apoptotic stimulus.Journal of cell science · 2020Article
- Understanding MAPK Signaling Pathways in Apoptosis.International journal of molecular sciences · 2020Review
- Increased glutamate transporter-associated anion currents cause glial apoptosis in episodic ataxia 6.Brain communications · 2020Article
- Cytotoxic effect of protic ionic liquids in HepG2 and HaCat human cells:Toxicology research · 2019Article
- Stress-induced modulation of volume-regulated anions channels in human alveolar carcinoma cells.Physiological reports · 2018Article
- Downregulation of LRRC8A protects human ovarian and alveolar carcinoma cells against Cisplatin-induced expression of p53, MDM2, p21Waf1/Cip1, and Caspase-9/-3 activation.American journal of physiology. Cell physiology · 2016Article
- Monitoring the progression of cell death and the disassembly of dying cells by flow cytometry.Nature protocols · 2016Article
- Regulation of p53 in NIH3T3 mouse fibroblasts following hyperosmotic stress.Physiological reports · 2015Article
- An in vitro model of skeletal muscle volume regulation.PloS one · 2015Article
- Osmostress-induced apoptosis in Xenopus oocytes: role of stress protein kinases, calpains and Smac/DIABLO.PloS one · 2015Article
- Anoctamin 6 differs from VRAC and VSOAC but is involved in apoptosis and supports volume regulation in the presence of Ca2+.Pflugers Archiv : European journal of physiology · 2014Article
- Ion channels and transporters in the development of drug resistance in cancer cells.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014Review
- Synthesis, physicochemical characterization, and cytocompatibility of bioresorbable, dual-gelling injectable hydrogels.Biomacromolecules · 2014Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell shrinkage is a hallmark of the apoptotic mode of programmed cell death, but it is as yet unclear whether a reduction in cell volume is a primary activation signal of apoptosis. Here we studied the effect of an acute elevation of osmolarity (NaCl or sucrose additions, final osmolarity 687 mosmol l(-1)) on NIH 3T3 fibroblasts to identify components involved in the signal transduction from shrinkage to apoptosis. After 1.5 h the activity of caspase-3 started to increase followed after 3 h by the appearance of many apoptotic-like bodies. The caspase-3 activity increase was greatly enhanced in cells expressing a constitutively active G protein, Rac (RacV12A3 cell), indicating that Rac acts upstream to caspase-3 activation. The stress-activated protein kinase, p38, was significantly activated by phosphorylation within 30 min after induction of osmotic shrinkage, the phosphorylation being accelerated in fibroblasts overexpressing Rac. Conversely, the activation of the extracellular signal-regulated kinase (Erk1/2) was initially significantly decreased. Subsequent to activation of p38, p53 was activated through serine-15 phosphorylation, and active p53 was translocated from the cytosol to the nucleus. Inhibition of p38 in Rac cells reduced the activation of both p53 and caspase-3. After 60 min in hypertonic medium the rate constants for K+ and taurine efflux were increased, particular in Rac cells. We suggest the following sequence of events in the cell shrinkage-induced apoptotic response: cellular shrinkage activates Rac, with activation of p38, followed by phosphorylation and nuclear translocation of p53, resulting in permeability increases and caspase-3 activation.
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