Abstract

Introduction

Materials & Methods

Results

Discussion & Conclusion

References

Discussion
Board

Normal human fibroblasts exhibit a finite proliferative potential in culture, which is referred to as in vitro cell aging. Recent molecular analyses have revealed many changes in gene expression as the cells enter the senescent phase. Among which, upregulations of Cdk inhibitors, such as sdi1(p21) and p16, are candidates for senescent growth arrest. We previously cloned p21 as a growth inhibitory gene from senescent cells. The transcriptional overexpression of p21, as well as p16 was attributed to a major causative mechanism underlying sensecent growth arrest. Therefore, putative transcriptional activators of such genes may control the proliferative potential. However, antisense or knock out experiments with the p21 gene revealed that other factor(s) were also required for the maintenance of senescence. Signals from telomere shortening or DNA methylation changes during successive rounds of DNA replication may also cause cells to exit the cell cycle. The molecular link between actual cell cycle arrest and the mechanism for counting cell division is still unclear.

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Presentation Number SAnoda0326
Keywords: cell aging, sensecence, growth arrest, Cdk inhibitor, cell cycle