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Open Access Research

The expression signature of in vitro senescence resembles mouse but not human aging

Kristian Wennmalm1, Claes Wahlestedt1 and Ola Larsson12*

Author Affiliations

1 Center for Genomics and Bioinformatics, Karolinska Institutet, Berzelius väg 35, 171 77 Stockholm, Sweden

2 University of Minnesota, Department of Medicine, Minneapolis, MN 55455, USA

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Genome Biology 2005, 6:R109  doi:10.1186/gb-2005-6-13-r109

Published: 16 December 2005

Abstract

Background

The biological mechanisms that underlie aging have not yet been fully identified. Senescence, a phenomenon occurring in vitro, limits the number of cell divisions in mammalian cell cultures and has been suggested to contribute to aging.

Results

We investigated whether the changes in gene expression that occur during mammalian aging and induction of cellular senescence are similar. We compared changes of gene expression in seven microarray datasets from aging human, mouse and rat, as well as four microarray datasets from senescent cells of man and mouse. The datasets were publicly available or obtained from other laboratories. Correlation measures were used to establish similarities of the expression profiles and gene ontology analyses to identify functional groups of genes that are co-regulated. Robust similarities were established between aging in different species and tissues, indicating that there is an aging transcriptome. Although some cross-species comparisons displayed high correlation, intra-species similarities were more reliable. Similarly, a senescence transcriptome was demonstrated that is conserved across cell types. A similarity between the expression signatures of cellular senescence and aging could be established in mouse, but not in human.

Conclusion

Our study is the first to use microarray data from several studies and laboratories for dissection of a complex biological phenotype. We demonstrate the presence of a mammalian aging transcriptome, and discuss why similarity between cellular senescence and aging is apparent in aging mice only.