In-vitro circadian rhythm of murine bone marrow progenitor production

Bourin, Philippe; Ledain, A.; Beau, J Le; Mille, Dominique; Lévi, Françis

doi:10.1081/cbi-120002677

Cited by 27 publications

(18 citation statements)

References 25 publications

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“…The ability of peripheral oscillators to maintain circadian rhythms in the absence of a central pacemaker has been further demonstrated as cultured fibroblasts displayed sustained rhythms in gene expression (3,17) and cultured murine bone marrow progenitors displayed sustained rhythms in response to hematopoietic growth factors (8). Nevertheless, these rhythms tended to fade away unless a stimulation (glucocorticoid, serum shock) or an environmental 24-h cycle (temperature, light) was introduced after a few days in culture, suggesting the need for a regular resetting of free-running peripheral oscillators in order for their coordination to be maintained (2,3,9,21,49).…”

Section: Discussionmentioning

confidence: 99%

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

Filipski

King²,

Etienne³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

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. Persistent twenty-four hour changes in liver and bone marrow despite suprachiasmatic nuclei ablation in mice. Am J Physiol Regul Integr Comp Physiol 287: R844 -R851, 2004. First published June 24, 2004 10.1152/ajpregu. 00085.2004.-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(Ϫ)], 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(Ϫ) 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 shamoperated and SCN(Ϫ) 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. circadian coordination; cancer chronotherapeutics; cortisol; cell cycle; dihydropyrimidine dehydrogenase APPROXIMATELY 25% of cancer patients displayed profound alterations of rest-activity pattern and cortisol rhythm independently of tumor stage or general condition (32-34). Poorer tumor response and shorter survival were reported in these patients compared with those with near normal circadian function (36,43). Such altered circadian function could also impair the therapeutic benefit that can result from chronotherapeutics, i.e., the delivery of anticancer treatments at selected times of day (12,23,26,27).This treatment optimization method is based on the regulation of cellular metabolism and proliferation by a molecular clock. This clock consists of interconnected molecular loops involving up to 12 specific clock genes. It has been uncovered in most mammalian tissues (21,35,41,42) and rhythmically regulates the transcription of 5-10% of the genome (14,21,41,42). Indeed, sustained rhythms in transcription or other cellular functions have been demonstrated in cultured mammalian cells, giving rise to the con...

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Section: Discussionmentioning

confidence: 99%

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

Filipski

King²,

Etienne³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Synchronized cell cultures display rhythmic transcription of drug metabolism and targets, such as Cyp2e1, Cyp3a4, and Top1 (90,203,204). Ex vivo cell cultures of bone marrow progenitors from male B6D2F1 or Balb/C mice show sustained circadian rhythms in pharmacodynamic response to granulo-monocytic colony-stimulating factor (GM-CSF) over 4 days (205). The circadian maximum in the proliferative response of bone marrow cells to GM-CSF occurs at the same circadian time in vitro and in vivo (205).…”

Section: Chronopharmacology At the Cellular Levelmentioning

confidence: 99%

Circadian Timing in Cancer Treatments

Lévi

Okyar

Dulong

et al. 2010

Annu. Rev. Pharmacol. Toxicol.

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The circadian timing system is composed of molecular clocks, which drive 24-h changes in xenobiotic metabolism and detoxification, cell cycle events, DNA repair, apoptosis, and angiogenesis. The cellular circadian clocks are coordinated by endogenous physiological rhythms, so that they tick in synchrony in the host tissues that can be damaged by anticancer agents. As a result, circadian timing can modify 2- to 10-fold the tolerability of anticancer medications in experimental models and in cancer patients. Improved efficacy is also seen when drugs are given near their respective times of best tolerability, due to (a) inherently poor circadian entrainment of tumors and (b) persistent circadian entrainment of healthy tissues. Conversely, host clocks are disrupted whenever anticancer drugs are administered at their most toxic time. On the other hand, circadian disruption accelerates experimental and clinical cancer processes. Gender, circadian physiology, clock genes, and cell cycle critically affect outcome on cancer chronotherapeutics. Mathematical and systems biology approaches currently develop and integrate theoretical, experimental, and technological tools in order to further optimize and personalize the circadian administration of cancer treatments.

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“…Samples from the bone marrow liquid culture were obtained every 3-4 hours for up to 4 days and exposed to granulocyte macrophage-colony-stimulating factor (GM-CSF) on agarose culture, a method used to determine the number of bone marrow GM progenitors. The study revealed proliferative circadian rhythms in cultured bone marrow cells that persisted for 3-4 days (Bourin et al 2002). Interestingly, the circadian maximum recurred daily near CT3, which is the time of peak ex vivo proliferative response of mouse bone marrow cells to GM-CSF exposure (Perpoint et al 1995).…”

Section: Circadian Gating Of Cell Divisionmentioning

confidence: 99%