scholarly journals Expression of mRNA for Adenosine A1, A2a, A2b, and A3 Receptors in HL-60 Cells: Dependence on Cell Cycle Phases

2011 ◽  
pp. 913-920 ◽  
Author(s):  
M. HOFER ◽  
L. DUŠEK ◽  
Z. HOFEROVÁ ◽  
L. STIXOVÁ ◽  
M. POSPÍŠIL
Keyword(s):  
Cell Cycle ◽  
Mrna Expression ◽  
S Phase ◽  
Cell Cycle Phase ◽  
Cycle Phase ◽  
Block Method ◽  
Physiological Mechanisms ◽  
Adenosine A1 ◽  
Adenosine A2a ◽  
Adenosine A2b

The present studies investigated changes in expression of mRNA for adenosine A1, A2a, A2b, and A3 receptors in samples of HL-60 promyelocytic cells differing in the actual presence of cells in various phases of the cell cycle induced by the double thymidine block method. Real-time PCR technique was used for obtaining data on mRNA expression. Statistical analysis of the data revealed that the mRNA expression of adenosine A1, A2a, and A3 receptors is dependent on the cell cycle phase. G0/G1 and G2/M phases were characterized by a higher mRNA expression of adenosine A1 receptors and a lower one of adenosine A2a and A3 receptors whereas the opposite was true for the S phase. Interestingly, expression of mRNA of the adenosine A2b receptors was independent on the cell cycle phase. The results indicate the plasticity of mRNA expression of adenosine receptors in the investigated promyelocytic cells and its interaction with physiological mechanisms of the cell cycle.

scholarly journals DNA damage checkpoint dynamics drive cell cycle phase transitions

2017 ◽  
Author(s):  
Hui Xiao Chao ◽  
Cere E. Poovey ◽  
Ashley A. Privette ◽  
Gavin D. Grant ◽  
Hui Yan Chao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Phase Transitions ◽  
Cell Cycle Progression ◽  
S Phase ◽  
Cell Cycle Phase ◽  
Cycle Phase ◽  
Dna Damage Checkpoint ◽  
Cycle Progression ◽  
Dna Damage Checkpoints

ABSTRACTDNA damage checkpoints are cellular mechanisms that protect the integrity of the genome during cell cycle progression. In response to genotoxic stress, these checkpoints halt cell cycle progression until the damage is repaired, allowing cells enough time to recover from damage before resuming normal proliferation. Here, we investigate the temporal dynamics of DNA damage checkpoints in individual proliferating cells by observing cell cycle phase transitions following acute DNA damage. We find that in gap phases (G1 and G2), DNA damage triggers an abrupt halt to cell cycle progression in which the duration of arrest correlates with the severity of damage. However, cells that have already progressed beyond a proposed “commitment point” within a given cell cycle phase readily transition to the next phase, revealing a relaxation of checkpoint stringency during later stages of certain cell cycle phases. In contrast to G1 and G2, cell cycle progression in S phase is significantly less sensitive to DNA damage. Instead of exhibiting a complete halt, we find that increasing DNA damage doses leads to decreased rates of S-phase progression followed by arrest in the subsequent G2. Moreover, these phase-specific differences in DNA damage checkpoint dynamics are associated with corresponding differences in the proportions of irreversibly arrested cells. Thus, the precise timing of DNA damage determines the sensitivity, rate of cell cycle progression, and functional outcomes for damaged cells. These findings should inform our understanding of cell fate decisions after treatment with common cancer therapeutics such as genotoxins or spindle poisons, which often target cells in a specific cell cycle phase.

DNA Damage Induced by DNA Topoisomerase I- and Topoisomerase II- Inhibitors Detected by Histone H2AX Phosphorylation in Leukemic Cells.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 4240-4240
Author(s):  
Dorota H. Halicka ◽  
Xuan Huang ◽  
Fevzi M. Ozkaynak ◽  
Karen Seiter ◽  
Frank Traganos ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Topoisomerase I ◽  
Caspase 3 ◽  
S Phase ◽  
Cell Cycle Phase ◽  
Cycle Phase ◽  
Dna Topoisomerase I ◽  
H2ax Phosphorylation ◽  
Dna Topoisomerase ◽  
Histone H2ax

Abstract Histone H2AX is phosphorylated on Ser-139 by ATM kinase in response to damage that induces dsDNA breaks. Immunocytochemical detection of phosphorylated H2AX (γH2AX), thus, reveals the presence of dsDNA breaks in chromatin. Multiparameter cytometry was presently used to correlate the appearance of γH2AX with: (a) cell cycle phase; (b) caspase-3 activation; and (c) apoptosis-associated DNA fragmentation in individual human leukemic HL-60 cells treated with the DNA topoisomerase I (topo1) inhibitors topotecan (TPT) and camptothecin (CPT) or with the topo2 inhibitor mitoxantrone (MTX). In response to TPT or CPT maximal increase of γH2AX immunofluorescence was seen in S-phase cells by 90 min. In contrast, following MTX treatment the maximal rise of γH2AX was detected at 2 h in G1 cells and the cell cycle phase specificity was much less apparent. A linear relationship between the drug concentration and increase of γH2AX immunofluorescence was seen only up to 200 nM TPT; a decline in γH2AX was apparent at a concentration range between 0.4 and 1.6 μM TPT. Thus, the intensity of γH2AX immunofluorescence, as a marker of cell survival following TPT treatment, can be used only within a limited range of drug concentration. Following treatment with TPT, CPT or MTX the peak of H2AX phosphorylation preceded caspase-3 activation and the appearance of apoptosis-associated DNA fragmentation, both selective to S-phase cells. Progression of apoptosis was paralleled by a decrease in γH2AX immunofluorescence. On the basis of our laboratory results, the present clinical study is evaluating ex vivo the feasibility of assessing DNA damage induced by treatment with topoisomerase inhibitors in patients with acute leukemias.

scholarly journals A cell-cycle-phase-specific mutant of amoeba

1984 ◽  
Vol 68 (1) ◽  
pp. 95-111
Author(s):  
A. Gangopadhyay ◽  
S. Chatterjee
Keyword(s):  
Cell Cycle ◽  
Cell Size ◽  
Size Structure ◽  
S Phase ◽  
Cell Cycle Phase ◽  
Membrane Properties ◽  
Cycle Phase ◽  
Mutagenic Action ◽  
A Cell ◽  
Characteristic Features

The treatment of Amoeba indica with ethylmethanesulphonate (EMS) at early S, late S and late G2 phases of the cell cycle leads to the production of mini amoeba cells in the G2 period. Among them, only a few of the mini cells that originated from EMS treatment at early S phase have been found to be viable and to give rise to stable clones. These mini amoebae show stable and altered characteristic features in cell size, structure, membrane properties, cell-cycle timing and the patterns of macromolecular syntheses as compared to the parental cells. It is suggested that the mini amoeba cell is a size mutant that has a cell-cycle-phase-specific origin. The finding is discussed in relation to preferential mutagenic action involving the functional state of DNA leading to the production of viable mutant amoebae.

Persistent twenty-four hour changes in liver and bone marrow despite suprachiasmatic nuclei ablation in mice

2004 ◽  
Vol 287 (4) ◽  
pp. R844-R851 ◽  
Author(s):  
Elisabeth Filipski ◽  
Verdun M. King ◽  
Marie-Christine Etienne ◽  
XiaoMei Li ◽  
Bruno Claustrat ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Bone Marrow ◽  
Body Temperature ◽  
Mrna Expression ◽  
Phase Distribution ◽  
Cell Cycle Phase ◽  
Cycle Phase ◽  
Suprachiasmatic Nuclei ◽  
Cell Cycle Phase Distribution ◽  
Rest Activity

Rest-activity or cortisol rhythms can be altered in cancer patients, a condition that may impair the benefits from a timed delivery of anticancer treatments. In rodents, the circadian pattern in rest-activity is suppressed by the destruction of the suprachiasmatic nuclei (SCN) in the hypothalamus. We sought whether such ablation would result in a similar alteration of cellular rhythms known to be relevant for anticancer drug chronopharmacology. The SCN of 77 B6D2F1 mice synchronized with 12 h of light and 12 h of darkness were destroyed by electrocoagulation [SCN(−)], while 34 animals were sham operated. Activity and body temperature were recorded by telemetry. Blood and organs were sampled at one of six circadian times for determinations of serum corticosterone concentration, blood leukocyte count, reduced glutathione (GSH), and dihydropyrimidine dehydrogenase (DPD) mRNA expression in liver and cell cycle phase distribution of bone marrow cells. Sham-operated mice displayed significant 24-h rhythms in rest-activity and body temperature, whereas such rhythms were found in none and in 15% of the SCN(−) mice, respectively. SCN lesions markedly altered the rhythmic patterns in serum corticosterone and liver GSH, which became nonsinusoidal. Liver DPD mRNA expression and bone marrow cell cycle phase distribution displayed similar 24-h sinusoidal patterns in sham-operated and SCN(−) mice. These results support the existence of another light-dark entrainable pacemaker that can coordinate cellular functions in peripheral organs. They suggest that the delivery of anticancer treatments at an optimal time of day may still be beneficial, despite suppressed rest-activity or cortisol rhythms.

Growth and cell cycle phase composition of fibroblasts in the reconstituted dermis model.

1990 ◽  
Vol 52 (5) ◽  
pp. 986-992
Author(s):  
Takeshi KONO ◽  
Tsukasa TANII ◽  
Masayoshi FURUKAWA ◽  
Nobuyuki MIZUNO ◽  
Shoji TANIGUCHI ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Phase Composition ◽  
Cell Cycle Phase ◽  
Cycle Phase

MITOMYCIN C INDUCED APOPTOSIS: INFLUENCE OF CELL CYCLE PHASE

1996 ◽  
Vol 88 (1-2) ◽  
pp. 82-82a ◽  
Author(s):  
Magali OLIVIER ◽  
Charles THEILLET
Keyword(s):  
Cell Cycle ◽  
Mitomycin C ◽  
Cell Cycle Phase ◽  
Cycle Phase ◽  
Induced Apoptosis
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