title: Regulatory volume decrease is actively modulated during the cell cycle.
abstract: Nasopharyngeal carcinoma cells, CNE-2Z, when swollen by 47% hypotonic solution, exhibited a regulatory volume decrease (RVD). The RVD was inhibited by extracellular applications of the chloride channel blockers tamoxifen (30 microM; 61% inhibition), 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB, 100 microM; 60% inhibition), and ATP (10 mM; 91% inhibition). The level and time constant of RVD varied greatly between cells. Most cells conducted an incomplete RVD, but a few had the ability to recover their volume completely. There was no obvious correlation between cell volume and RVD capacity. Flow cytometric analysis showed that highly synchronous cells were obtained by the mitotic shake-off technique and that the cells progressed through the cell cycle synchronously when incubated in culture medium. Combined application of DNA synthesis inhibitors, thymidine and hydroxyurea arrested cells at the G1/S boundary and 87% of the cells reached S phase 4 h after being released. RVD capacity changed significantly during the cell cycle progression in cells synchronized by shake-off technique. RVD capacity being at its highest in G1 phase and lowest in S phase. The RVD capacity in G1 (shake-off cells sampled after 4 h of incubation), S (obtained by chemical arrest), and M cells (selected under microscope) was 73, 33, and 58%, respectively, and the time constants were 435, 769, and 2,000 sec, respectively. We conclude that RVD capacity is actively modulated in the cell cycle and RVD may play an important role in cell cycle progress.
authors.affiliation: School of Biosciences, Cardiff University, Cardiff, United Kingdom.
authors.forename: Liwei
authors.initials: L
authors.lastname: Wang
authors.forename: Lixin
authors.initials: L
authors.lastname: Chen
authors.forename: Linyan
authors.initials: L
authors.lastname: Zhu
authors.forename: Michelle
authors.initials: M
authors.lastname: Rawle
authors.forename: Sihuai
authors.initials: S
authors.lastname: Nie
authors.forename: Jin
authors.initials: J
authors.lastname: Zhang
authors.forename: Zhong
authors.initials: Z
authors.lastname: Ping
authors.forename: Cai
authors.initials: C
authors.lastname: Kangrong
authors.forename: Tim J C
authors.initials: TJ
authors.lastname: Jacob
mesh_terms: D000255:Adenosine Triphosphate / Q000494:pharmacology; D002277:Carcinoma / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology*; D002453:Cell Cycle / Q000187:drug effects / Q000502:physiology; D048429:Cell Size / Q000187:drug effects / Q000502:physiology; D018118:Chloride Channels / Q000037:antagonists & inhibitors; D005434:Flow Cytometry; D016193:G1 Phase / Q000187:drug effects; D006801:Humans; D006918:Hydroxyurea / Q000494:pharmacology; D007038:Hypotonic Solutions / Q000494:pharmacology; D008938:Mitosis / Q000187:drug effects; D009303:Nasopharyngeal Neoplasms / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology*; D009579:Nitrobenzoates / Q000494:pharmacology; D019384:Nucleic Acid Synthesis Inhibitors / Q000494:pharmacology; D016196:S Phase / Q000187:drug effects; D013629:Tamoxifen / Q000494:pharmacology; D013936:Thymidine / Q000494:pharmacology; D014407:Tumor Cells, Cultured
chemical_list: D018118:Chloride Channels; D007038:Hypotonic Solutions; D009579:Nitrobenzoates; D019384:Nucleic Acid Synthesis Inhibitors; D013629:Tamoxifen; C058176:5-nitro-2-(3-phenylpropylamino)benzoic acid; D000255:Adenosine Triphosphate; D013936:Thymidine; D006918:Hydroxyurea