ArticleThe Journal of physiology2016
Adaptive responses of cell hydration to a low temperature arrest.
Article in The Journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Carbohydrate-Mediated Cellular Uptake of Boronic Acid Hybrids In Cellulo and Insulin-Deficient Zebrafish: Live Imaging and Application of Multiphoton FLIM.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Fluorescent naphthalimide boronates as theranostics: structural investigations, confocal fluorescence and multiphoton fluorescence lifetime imaging microscopy in living cells.RSC chemical biology · 2023Article
- Hypertonicity-induced cation channels in HepG2 cells: architecture and role in proliferation vs. apoptosis.The Journal of physiology · 2018Article
- Modification of cellular membranes conveys cryoprotection to cells during rapid, non-equilibrium cryopreservation.PloS one · 2018Article
- Channelling frozen cells to survival after thawing: opening the door to cryo-physiology.The Journal of physiology · 2016Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Slow cooling leads to a passive dehydration of cells, whereas rehydration during warming reflects the active regain of functionality. The ability to modulate such an energy demanding process could be instrumental in optimizing the cryo-arrest of living systems. In the present study, various levels of hypertonic stress were used to disturb the water content of cells and to define the energy profiles of aquaporins and (Na(+) conducting) cation channels during rehydration. Na(+) import was found to be the rate-limiting step in water restoration, whereas aquaporins merely played a permissive role. Indeed, regulated Na(+) import was increased 2-fold following cryo-arrests, thus facilitating the osmotic rehydration of cells. Freezing temperatures increased cell viscosity with a remarkable hysteresis and viscosity was a trigger of cation channels. The peptide hormone vasopressin was a further activator of channels, increasing the viability of post-cryo cells considerably. Hence, the hormone opens the path for a novel class of cryo-protectants with an intrinsic biological activity.
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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.