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. 2014 Oct 22;58(4):2444. doi: 10.4081/ejh.2014.2444

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©Copyright L.V. Renna et al.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 5. — DM premature senescence pathway. A) Representative western blot analyses of p16 in the early (e) and late (l) stages of myoblast proliferative lifespan; the results have been normalized to the expression of β-tubulin. B) Histograms representing mean values of p16 protein expression analysed by densitometry in healthy (CTR; n=4), DM1 (n=3) and DM2 (n=4) patients; at both stages analyzed, p16 was more expressed in DM1 cells as compared to the controls while the expression was similar in DM2 and control myoblasts; scale bars represent SEM. C) Mean length of telomeric restriction fragments (TRF) measured on DM2 (n=4) and control (n=4) myoblasts at proliferative and senescent stage; senescent DM2 cells had shorter telomeres than the proliferating cells (*P<0.05); scale bars represent SEM. D) Mean length (in bps) of telomeric DNA lost per division in control and DM2 myoblasts; DM2 cells lost more bps per division than control cells; scale bars represent SEM.