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Protective effects of telomerase on H2O2 induced cellular senescence

The exact mechanism(s) of cellular aging is not clear. After a finite number of cell divisions, normal cultured human cells enter a state of irreversible growth arrest, termed “replicative senescence”. Alternatively, oxidative stress in the form of hydrogen peroxide (H2O2) can render human fibroblasts nonproliferative and quiescent, a phenomenon known as stress‐induced premature senescence (SIPS). To investigate the underlying mechanism of this accelerated aging phenomenon, the telomerase gene in human normal fibroblasts was overexpressed. The cells with stable transfected telomerase gene expressed high telomerase activity comparing to their controls. The transfected normal fibroblasts cells with high telomerase activity all reached immortality (beyond 350 passages), but replicative senescence still existed in the vector‐only‐control. In terms of telomere length, telomerase gene overexpressed fibroblasts showed very little telomere shortening with aging. Interestingly, by using H2O2 treatment, both the vector‐only‐control fibroblasts and telomerase‐gene‐ overexpressed fibroblasts showed elevated β‐galactosidase staining, a sign of cellular senescence. However, the sign of senescence was more dramatic in vector‐only‐controls as compared to telomerase‐overexpressed cells. In addition, MnSOD expression in telomerase‐overexpressed‐fibroblasts was increased much more than their control cells after H2O2 treatments. Likewise, G6PD expression was higher in telomerase‐overexpressed‐fibroblasts than their control cells with or without H2O2 treatment. Taken together, these data support the notion that both telomere shortening and oxidative stress are important driving force of cellular senescence.