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Home | Pregnancy Timeline | News Alerts |News Archive Jan 14, 2015

The circadian clock regulates metabolism in epidermal stem cells visible in the high NADH/NAD+ ratio, or as increased glycolysis found at night. This high ratio relates to a higher proportion of stem cells in the S phase of cell division. Image Credit: University of California, Irvine

 






 

 

Circadian rhythms regulate skin stem cell function?

The body clock in mice protects cells from oxygen damage during cell division — which may be true in humans as well.

University of California, Irvine (UC Irvine) scientists studying the role of circadian rhythms in skin stem cells found that this clock plays a key role in coordinating daily metabolic cycles and cell division.

Their research, which appears in Cell Reports, shows for the first time how the body's intrinsic day-night cycles protect and nurture stem cell differentiation. Furthermore, this work offers novel insights into a mechanism whereby an out of synch circadian clock can contribute to accelerated skin aging and cancers.

Bogi Andersen, professor of biological chemistry and medicine, and Enrico Gratton, professor of biomedical engineering, focused their efforts on the epidermis, the outermost protective layer of the skin that is maintained and healed by long-lived stem cells.


While the role of the circadian clock in processes such as sleep, feeding and all metabolism linked to feeding and fasting are well known, very little is known if the circadian clock also regulates stem cell functions.


The researchers made sensitive and quantitative measurements of the metabolic state of individual cells within living tissue and discovered that the circadian clock regulates one form of metabolism in these stem cells, known as oxidative phosphorylation. This type of metabolism creates oxygen radicals that can damage DNA and other components of the cell. In fact, one theory of aging suggests that aging is caused by accumulated damage from metabolism-generated oxygen radicals in stem cells.

The study found that the circadian clock within stem cells shifts the timing of cell division to avoid damage to DNA during oxidative phosphorylation.


Past studies in animals have linked aging to disruption of circadian rhythms. Andersen believes that accelerated aging may be caused by unsynchronized cycles of metabolism and cell proliferation in stem cells.


"Our studies were conducted in mice, but the greater implication of the work relates to disruption of circadian rhythm as being very common in modern society. One consequence of such disruption could be abnormal function of stem cells and accelerated aging," Andersen added.

Highlights
•We used a noninvasive method to study epidermal stem cell metabolism in vivo
•The circadian clock regulates intermediary metabolism in epidermal stem cells
•A high NADH/NAD+ ratio, reflecting increased glycolysis, is found during the night
•This high NADH/NAD+ ratio correlates with a higher proportion of stem cells in S phase

Summary
Through the use of bulk measurements in metabolic organs, the circadian clock was shown to play roles in organismal energy homeostasis. However, the relationship between metabolic and circadian oscillations has not been studied in vivo at a single-cell level. Also, it is unknown whether the circadian clock controls metabolism in stem cells. We used a sensitive, noninvasive method to detect metabolic oscillations and circadian phase within epidermal stem cells in live mice at the single-cell level. We observe a higher NADH/NAD+ ratio, reflecting an increased glycolysis/oxidative phosphorylation ratio during the night compared to the day. Furthermore, we demonstrate that single-cell metabolic heterogeneity within the basal cell layer correlates with the circadian clock and that diurnal fluctuations in NADH/NAD+ ratio are Bmal1 dependent. Our data show that, in proliferating stem cells, the circadian clock coordinates activities of oxidative phosphorylation and glycolysis with DNA synthesis, perhaps as a protective mechanism against genotoxicity.

This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/3.0/).

Authors: Chiara Stringari, Hong Wang, Mikhail Geyfman and Viera Crosignani with UCI; and Vivek Kumar and Joseph S. Takahashi.

University of Texas Southwestern Medical Center in Dallas contributed to the study, which received support from the National Institutes of Health (grants R01 AR056439, P50 GM076516 and P41 GM103540).

DOI: http://dx.doi.org/10.1016/j.celrep.2014.12.007


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