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This research investigates the activation of atypical DNA damage response mechanisms in senescent cells without actual DNA damage.

December 15, 2009Cell CycleOpen Access

Pseudo-DNA damage response in senescent cells

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Randomized trial demonstrates atypical DNA damage responses in senescent cells, suggesting new biomarker potential.

This research investigates the activation of atypical DNA damage response mechanisms in senescent cells without actual DNA damage.
Utilized sodium butyrate to induce p21 and ectopic expression of p21 and p16 to stimulate senescence.
Assessed DNA damage response markers such as gammaH2AX foci and p-ATM nuclear staining.
Employed rapamycin to evaluate its effects on gammaH2AX foci formation in senescent cells.
Sodium butyrate-induced senescence showed no detectable DNA breaks but activated atypical DDR markers.
Senescent cells displayed gammaH2AX foci and p-ATM staining but lacked accumulation of 53BP1 in these foci.
Rapamycin treatment significantly reduced gammaH2AX foci formation in senescent cells.

Pospelova et al. (2009) studied this question.

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