Both authors contributed equally to this work.
Metabolic and Steatohepatitis
Depending on the stage of hepatosteatosis, p53 causes apoptosis primarily through either DRAM-induced autophagy or BAX
Version of Record online: 12 AUG 2013
© 2013 The Authors. Liver International published by John Wiley & Sons Ltd.
This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
Volume 33, Issue 10, pages 1566–1574, November 2013
How to Cite
Liver Int. 2013; 33: 1566–1574
- Issue online: 6 OCT 2013
- Version of Record online: 12 AUG 2013
- Accepted manuscript online: 16 JUN 2013 05:53AM EST
- Manuscript Accepted: 28 MAY 2013
- Manuscript Revised: 23 MAY 2013
- Manuscript Received: 20 DEC 2012
- National Natural Science Foundation of China. Grant Numbers: 81071843, 81272266, 30910103915
- Basic-Clinical Collaborative Research Fund
- CCMU. Grant Number: 12JL-L05
- Beijing Institute of Hepatology. Grant Number: BJIH-01201
Fig. S1. Different concentrations of OA induce lipid accumulation and LDH release differently. HepG2 cells were cultured in 24-well plates for 24 h with 400, 800 or 1200 μM OA. The levels of intracellular triglycerides and released LDH in the HepG2 cells in response to the OA stimulus were analyzed. Data (mean ± SEM) represent three independent experiments. Significance levels were P < 0.05 and P < 0.01 at 24 h.
Fig. S2. The effects of autophagy inhibition by LY294002 pretreatment on OA-induced lipid accumulation and LDH release. HepG2 cells were pretreated with LY294002 for 5 h to inhibit autophagy and then treated with 400, 800 or 1200 μM OA for 24 h. The levels of intracellular triglycerides and released LDH were analyzed. Data (mean cells ± SEM) represent three independent experiments. The significance level was P < 0.05 at 24 h.
Please note: Wiley Blackwell is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.