Supplementary Materials

Supplementary Material for:

Characterization of the molecular mechanisms underlying increased ischemic damage in the aldehyde dehydrogenase 2 genetic polymorphism using a human induced pluripotent stem cell model system

Antje D. Ebert, Kazuki Kodo, Ping Liang, Haodi Wu, Bruno C. Huber, Johannes Riegler, Jared Churko, Jaecheol Lee, Patricia de Almeida, Feng Lan, Sebastian Diecke, Paul W. Burridge, Joseph D. Gold, Daria Mochly-Rosen,* Joseph C. Wu*

*Corresponding author. E-mail: joewu{at}stanford.edu (J.C.W.); mochly{at}stanford.edu (D.M.-R.)

Published 24 September 2014, Sci. Transl. Med. 6, 255ra130 (2014)
DOI: 10.1126/scitranslmed.3009027

This PDF file includes:

  • Methods
  • Fig. S1. Effect of 4-MP and daidzin on ALDH2 activity in cell lysates from ALDH2*2/1 and wild-type fibroblasts.
  • Fig. S2. ROS are enhanced upon external challenge with 4HNE in ALDH2*2/1 fibroblasts, but not in wild-type control.
  • Fig. S3. Alda-1 and 4HNE do not interfere with Amplex Red–based analysis of xanthine oxidase–catalyzed H2O2 formation.
  • Fig. S4. Characterization of a human iPSC model for the ALDH2*2/1 genetic polymorphism.
  • Fig. S5. ALDH2*2/1 and wild-type iPSCs form teratoma and present a regular karyotype.
  • Fig. S6. Profiling of ALDH2*2/1 and wild-type control iPSC-CMs.
  • Fig. S7. Electrophysiological analysis of ALDH2*2/1 and wild-type iPSC-CMs reveals typical profiles.
  • Fig. S8. ALDH2*2/1 iPSC-CMs express equal levels of ALDH2 compared to wild-type control.
  • Fig. S9. Effect of an unrelated ROS scavenger, catalase, on total cellular ROS levels in postischemic ALDH2*2/1 iPSC-CMs, compared to wild-type control.
  • Fig. S10. Analysis of differences in mitochondrial-based metabolism comparing ALDH2*2/1 iPSC-CMs versus wild-type control iPSC-CMs.
  • Fig. S11. Metabolic profiling in ALDH2*2/1 and wild-type iPSC-CMs.
  • Fig. S12. Validation of relative transcriptome changes for selected target genes in ALDH2*2/1 and wild-type iPSC-CMs, comparing control (normoxia) and postischemia.
  • Table S1. Overview on profiling assays performed for characterization of iPSCs.
  • Table S2. Overview on profiling assays performed for characterization of iPSCCMs.
  • Table S3. Quantification and detailed parameters of experiments shown in fig. S4.
  • Table S4. Canonical pathways and corresponding fold changes [–log (P value)] displayed in Fig. 4A.
  • Table S5. Canonical pathways and corresponding fold changes [–log (P value)] displayed in Fig. 4B.
  • Table S6. Increased levels of p-JNK in post-ischemic ALDH2*2/1 iPSC-CMs are reduced by JNK inhibition (JIP) and ALDH2 activation (Alda-1).
  • Legends for videos S1 and S2

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Other Supplementary Material for this manuscript includes the following:

  • Video S1 (.wmv format). Contracting monolayer of control wild-type iPSC-CMs.
  • Video S2 (.wmv format). Contracting monolayer of ALDH2*2/1 iPSC-CMs.

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