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1 Department of Pathophysiology, University Medical School, Poznan, Poland
2 Laboratory for Molecular Bases of Aging, Nencki Institute of Experimental Biology, Warsaw, Poland
3 Department of Histology and Embryology, University Medical School, Poznan, Poland
4 Department of Nephrology and Medical Intensive Care, Universitatsmedizin Charite, Berlin, Germany
5 Department of Pathophysiology, University Medical School, Poznan, Poland; Department of Nephrology and Medical Intensive Care, Universitatsmedizin Charite, Berlin, Germany
* To whom correspondence should be addressed. E-mail: jwitow{at}amp.edu.pl.
Background: Much has been learned about the mechanisms underlying cellular senescence. The pathways leading to senescence appear to vary depending on the cell type and cell culture conditions. In this respect, little is known about senescence of human peritoneal mesothelial cells (HPMC). Previous studies have significantly differed in the reported proliferative lifespan of HPMC. Therefore, in the present study we have examined how HPMC enter state of senescence under conditions typically used for HPMC culture. Methods: HPMC were isolated from omentum and grown into senescence. The cultures were assessed for the growth rate, the presence of senescence markers, activation of cell-cycle inhibitors, and the oxidative stress. Results: HPMC were found to reach on average 6 population doublings prior to senescence. The terminal growth arrest was associated with decreased expression of Ki67 antigen, increased percentage of cells in the G1 phase, reduced EPC-1 mRNA expression, and the presence of senescence-associated 
-galactosidase (SA--Gal). Compared to early-passage cells, the late-passage HPMC exhibited increased expression of p16INK4a but not of p21Cip1. In addition, these cells generated more reactive oxygen species and displayed increased presence of oxidatively modified DNA (8-OH-dG). Conclusion: These results demonstrate that early onset of senescence in omentum-derived HPMC may be associated with oxidative stress-induced up-regulation of p16INK4a.
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