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A role for 1α,25-dihydroxyvitamin D3 in the expression of circadian genes

  • Instituto Tecnologico de Estudios Superiores de Monterrey
    ,
  • Catedra de Terapia Celular
Research Output:
Contribution to journal
Article
Peer-review

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Scopus
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SciVal
FWCI
1.20
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Author count
4
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Citations
42
SciVal
Paper percentile
75

Abstract

The active form of vitamin D, 1α,25-(OH)2D3, has been associated with metabolism control, cell growth, differentiation, antiproliferation, apoptosis, and adaptive/innate immune responses, besides its functions in the integrity of bone and calcium homeostasis. The circadian rhythm regulates a variety of biological processes, many of them related to the functions associated with 1α,25-(OH)2D3. In the present study, we determine whether 1α,25-(OH)2D3 alters the expression of circadian genes in adipose-derived stem cells (ADSCs). The effect of 1α,25-(OH)2D3 on the expression of circadian genes BMAL1 and PER2 was measured by qPCR, over a 60-h period every 4 h, in serum shocked ADSCs, serum shocked ADSCs supplemented with 1α,25-(OH)2D3, and ADSCs under the presence of only 1α,25-(OH)2D3. The results showed that 1α,25-(OH)2D3 was able to synchronize circadian clock gene expression in ADSCs. The expression of circadian genes BMAL1 and PER2 in ADSCs that contained only 1α,25-(OH)2D3 has a profile similar to that found in the ADSCs synchronized by a serum shock. The results suggest an important role of 1α,25-(OH)2D3 in the regulation of the molecular clock.

Publication Information

Output type

Research Output:
Contribution to journal
Article
Peer-review

Original language

English

Pages from-to (Number of pages)

Pages 384-388 (5 pages)

Journal (Volume, Issue Number)

Journal of Biological Rhythms (Volume 29, Issue 5)

Publication milestones

  • Published - 11/10/2014

Publication status

Published - 11/10/2014

ISSN

0748-7304

Publication IDs

  • Scopus: 84910053638
  • PubMed: 25231949

Funding Details

Gutierrez-Monreal and Cuevas-Diaz express their gratitude to the Mexican National Council for Science and Technology (CONACYT) for the PhD grants scholarship CVU269963 and CVU359186, respectively. This work was funded by Catedra de Hematologia y Cancer and Catedra de Terapia Celular from the Tecnologico de Monterrey.
FundersFunding numbers
CONACYT
CVU269963, CVU359186
ITESM
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