Research Paper Volume 13, Issue 9 pp 12334—12358

The nuclear sirtuin SIRT6 protects the heart from developing aging-associated myocyte senescence and cardiac hypertrophy

Sirt6 overexpression protects cardiomyocytes from mitochondrial and telomere DNA damage. (A) Relative mitochondrial DNA lesions in the control and senescence induced cardiomyocytes transduced with or without SIRT6. Values are the average of three independent experiments, Mean ± SE. (B) Relative telomere length in the control and senescence induced cardiomyocytes transduced with empty or SIRT6 adenovirus. Values are the average of three independent experiments. Mean ± SE. (C) H9c2 cardiomyocytes were treated with doxorubicin in the presence or absence of SIRT6 to induce senescence. Cell lysate was prepared and analyzed by immunoblotting using indicated antibodies. Representative blot of three independent experiments showing two different samples in each group (quantification of blots is given in Supplementary Figure 5A–5G).

Figure 5. Sirt6 overexpression protects cardiomyocytes from mitochondrial and telomere DNA damage. (A) Relative mitochondrial DNA lesions in the control and senescence induced cardiomyocytes transduced with or without SIRT6. Values are the average of three independent experiments, Mean ± SE. (B) Relative telomere length in the control and senescence induced cardiomyocytes transduced with empty or SIRT6 adenovirus. Values are the average of three independent experiments. Mean ± SE. (C) H9c2 cardiomyocytes were treated with doxorubicin in the presence or absence of SIRT6 to induce senescence. Cell lysate was prepared and analyzed by immunoblotting using indicated antibodies. Representative blot of three independent experiments showing two different samples in each group (quantification of blots is given in Supplementary Figure 5A5G).