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. 2012 Jul 27;21(21):4680–4702. doi: 10.1093/hmg/dds309

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© The Author 2012. Published by Oxford University Press

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 11. — Impaired autophagic turnover triggers caspase-3 over-activation in cells harboring mitochondrial deficits. Caspase-3 activation was addressed by Ac-DEVD-pNA cleavage in CT and sPD cybrids (A) (n= 12; ***P< 0.001, versus CT cybrids); NT2 Rho0 cells (B) (n= 5; **P< 0.01, ***P< 0.001, versus untreated Rho0 cells) treated with or without lysosomal inhibitors (NL), 3-MA or rapamycin (Rap) for 4 h; and in MPP⁺-treated NT2 Rho+ cells treated with or without 3-MA for 4 h (C) (n= 6–8; *P< 0.001, versus untreated cells; ^###P< 0.001, versus MPP⁺-treated cells; ^&&P< 0.01, versus 3-MA-treated cells) or Rap for 6 h (D) as indicated (n= 6–8; ***P< 0.001, versus untreated cells; ^#P< 0.01, versus Rap-treated cells; ^&&&P< 0.001, versus MPP⁺-treated cells).