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. Author manuscript; available in PMC: 2011 Jul 1.
Published in final edited form as: Hepatology. 2010 Jul;52(1):266–277. doi: 10.1002/hep.23645

Fig. 2.

Fig. 2

Cell death in menadione-treated siAtg5 cells is caspase dependent and associated with activation of the mitochondrial death pathway. (A) Protein was isolated from VEC and siAtg5 cells untreated or treated with 50 μM menadione for the indicated number of hours. Aliquots of protein were immunoblotted with antibodies for caspase 3 (Casp 3), caspase 7 (Casp 7), poly-ADP ribose polymerase (PARP) and β-actin as a loading control. Arrow indicates the cleaved form of PARP. (B) Percentage cell death in VEC and siAtg5 cells treated with 50 or 60 μM menadione after pretreatment with the vehicle dimethyl sulfoxide (DMSO) or Q-VD-OPh (QVD) (*P<0.0001 as compared to DMSO-treated cells; n=4). (C) Immunoblots of mitochondrial protein isolates from VEC and siAtg5 cells untreated or treated with 50 μM menadione for the indicated number of hours. Proteins were immunoblotted with antibodies for cytochrome c (Cyt c), Bid, Bax, and cytochrome oxidase (Cyt ox). tBid is indicated by the arrow. (D) Immunoblots of cytosolic protein isolates from the same cells probed with the indicated antibodies.