The telomere lenght was also preserved in aged CalpTG mice in comparison to aged WT animals (Fig. 2M, p = 0.007). This could not be ascribed to an increased telomerase activity (Fig. 2N). To assess whether calpastatin transgene could by itself protect against replicative senescence, a culture of tubular cells from CalpTG and WT mice kidneys has been performed during 5 months. There was no difference in telomere length shortening or p21 expression in vitro, evidencing that the differences of telomere shortening observed in vivo result from cellular interactions with the environment, e.g. oxydative stress (Fig. 3A,B).Figure 3Calpastatin overexpression in tubular cells in vitro does not protect against aging. Prominin 1 positive proximal tubular cells have been isolated by flow cytometry and cultured during 5 months. After 12 passages, telomere lenght decreased similarly in cells from WT and CalpTG (TG) mice (A, n = 3). In addition, after 6 passages, a similar proportion of WT and CalpTG cells expressed p21, a classical marker of senescence (B, n = 3).