Research Papers:

Is senescence-associated β-galactosidase a marker of neuronal senescence?

Malgorzata Piechota _, Piotr Sunderland, Adrianna Wysocka, Maria Nalberczak, Malgorzata A. Sliwinska, Kasia Radwanska and Ewa Sikora

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Oncotarget. 2016; 7:81099-81109. https://doi.org/10.18632/oncotarget.12752

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Malgorzata Piechota1,*, Piotr Sunderland1,*, Adrianna Wysocka1,3, Maria Nalberczak2, Malgorzata A. Sliwinska2, Kasia Radwanska2, Ewa Sikora1

1Laboratory of Molecular Bases of Aging, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw 02-093, Poland

2Laboratory of Molecular Basis of Behavior, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw 02-093, Poland

3Laboratory of Preclinical Studies in Neurodegenerative Diseases, Nencki Institute of Experimental Biology, Polish Academy of Sciences, 02-093, Warsaw, Poland

*These authors have contributed equally to this study

Correspondence to:

Malgorzata Piechota, email: [email protected]

Keywords: aging, DNA damage response, neurons, senescence, SA-β-galactosidase

Received: June 08, 2016    Accepted: October 06, 2016    Published: October 19, 2016


One of the features of cellular senescence is the activity of senescence-associated- β-galactosidase (SA-β-gal). The main purpose of this study was to evaluate this marker of senescence in aging neurons. We found that cortical neurons exhibited noticeable SA-β-gal activity quite early in culture. Many SA-β-gal-positive neurons were negative for another canonical marker of senescence, namely, double-strand DNA breaks (DSBs). Moreover, DDR signalling triggered by low doses of doxorubicin did not accelerate the appearance of neuronal SA-β-gal. In vivo, we observed pronounced induction of SA-β-gal activity in the hippocampus of 24-month-old mice, which is consistent with previous findings and supports the view that at this advanced age neurons developed a senescence-like phenotype. Surprisingly however, relatively high SA-β-gal activity, probably unrelated to the senescence process, was also observed in much younger, 3-month-old mice. In conclusion, we propose that SA-β-gal activity in neurons cannot be attributed uniquely to cell senescence either in vitro or in vivo. Additionally, we showed induction of REST protein in aging neurons in long-term culture and we propose that REST could be a marker of neuronal senescence in vitro.

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