Over‐expression of circadian clock gene Bmal1 affects proliferation and the canonical Wnt pathway in NIH‐3T3 cells

Sep 11, 2012Cell biochemistry and function

Increased levels of the body’s clock gene Bmal1 influence cell growth and a key cell signaling pathway in NIH-3T3 cells

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Abstract

Bmal1 over-expression in NIH-3T3 cells resulted in increased cell proliferation rates.

Bmal1 is linked to circadian rhythms and may influence ageing features in mice.
Bmal1-/- mice displayed characteristics of premature ageing, including reduced bone mass.
Proliferation of bone marrow mesenchymal stem cells (BMSCs) and Bmal1 expression decreased with age.
A positive correlation may exist between Bmal1 protein levels and BMSC proliferation.
Increased expression of β-catenin, a key factor in the Wnt pathway, was observed following Bmal1 over-expression.

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Bmal1 is a transcription factor that plays a central role in the regulation of circadian rhythms. Recent study reported that Bmal1-/- mice displayed many known features of premature ageing, such as reduction of bone mass. Our previous study has found that both the proliferation of bone marrow mesenchymal stem cells (BMSCs) and Bmal1 expression decreased with advancing age. It seemed that a positive correlation existed between Bmal1 protein level and the proliferative activity of BMSCs. β-catenin, the core factor of the canonical Wnt pathway, also showed reduced expression in aged mice. In order to further confirm this, we constructed a lentiviral vector to over-express Bmal1 in NIH-3T3 cells; successful transfection was verified. The cell proliferation rate of infected cells was higher than the non-transfected NIH-3T3 cells, suggesting that circadian clock gene Bmal1 can promote proliferation. β-catenin showed an increased expression in NIH-3T3 cells after Bmal1 over-expression, indicating that activation of the canonical Wnt pathway might be the mechanism underlying the effect of circadian clock gene Bmal on promoting cell proliferation.

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Over‐expression of circadian clock gene Bmal1 affects proliferation and the canonical Wnt pathway in NIH‐3T3 cells

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