Supplementary Materials

Supplementary Materials for:

Increased activity of TNAP compensates for reduced adenosine production and promotes ectopic calcification in the genetic disease ACDC

Hui Jin, Cynthia St. Hilaire, Yuting Huang, Dan Yang, Natalia I. Dmitrieva, Alejandra Negro, Robin Schwartzbeck, Yangtengyu Liu, Zhen Yu, Avram Walts, Jean-Michel Davaine, Duck-Yeon Lee, Danielle Donahue, Kevin S. Hsu, Jessica Chen, Tao Cheng, William Gahl, Guibin Chen, Manfred Boehm*

*Corresponding author. Email: boehmm{at}nhlbi.nih.gov (M.F.); chengb{at}nhlbi.nih.gov (G.C.)

This PDF file includes:

  • Fig. S1. Reprogramming efficiency in ACDC fibroblasts.
  • Fig. S2. Representative karyotypes of ACDC iPSCs.
  • Fig. S3. Generation and characterization of ACDC iPSC lines overexpressing CD73.
  • Fig. S4. TNAP is not present in control human artery that is free from calcification.
  • Fig. S5. Schematic of differentiation of iPSCs into iMSCs.
  • Fig. S6. CD73 overexpression rescues osteogenic defects in ACDC iMSCs.
  • Fig. S7. Overexpression of CD73 decreases TNAP in ACDC iPSCs.
  • Fig. S8. Effect of AR agonists on calcification in teratomas.
  • Fig. S9. AR agonists do not affect teratoma size.
  • Fig. S10. TNAP activity in fibroblasts from control and ACDC patients.
  • Fig. S11. TNAP activity and calcification in hMSCs.
  • Fig. S12. Rapamycin treatment does not affect teratoma size.

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Citation: H. Jin, C. St. Hilaire, Y. Huang, D. Yang, N. I. Dmitrieva, A. Negro, R. Schwartzbeck, Y. Liu, Z. Yu, A. Walts, J.-M. Davaine, D.-Y. Lee, D. Donahue, K. S. Hsu, J. Chen, T. Cheng, W. Gahl, G. Chen, M. Boehm, Increased activity of TNAP compensates for reduced adenosine production and promotes ectopic calcification in the genetic disease ACDC. Sci. Signal. 9, ra121 (2016).

© 2016 American Association for the Advancement of Science