Supplementary Materials

The PDF file includes:

  • Methods
  • Fig. S1. Characterization of LMNA mutation family.
  • Fig. S2. Generation of iPSCs and differentiation of iPSC-ECs.
  • Fig. S3. Characterization of iPSC-ECs from healthy control and LMNA patients.
  • Fig. S4. Characterization of iPSC-ECs from additional healthy control and LMNA patients.
  • Fig. S5. Characterization of primary ECs isolated from LMNA patients.
  • Fig. S6. Generation and characterization of genome-edited iPSCs.
  • Fig. S7. Transcriptional characterization of iPSC-ECs.
  • Fig. S8. Characterization of iPSC-ECs under shear stress.
  • Fig. S9. Screening of small molecules that increase KLF2 expression in LMNA iPSC-ECs.
  • Fig. S10. Lovastatin improves EC function in LMNA iPSC-ECs.
  • Fig. S11. Lovastatin improves EC function in cardiolaminopathy patients.
  • Fig. S12. Lovastatin improves LMNA iPSC-CM phenotype when cocultured with LMNA iPSC-ECs.
  • Fig. S13. Lovastatin up-regulates genes responsible for cardiac mechanics in LMNA iPSC-CMs when cocultured with LMNA iPSC-ECs.
  • Fig. S14. Characterization of LMNA iPSC-CMs in inverse cocultures.
  • Fig. S15. Summary figure of modeling endothelial dysfunction in LMNA-related DCM using patient-specific iPSC-ECs.
  • Table S1. Demographic and clinical characteristics of healthy control and LMNA patients at baseline.
  • References (6163)

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Other Supplementary Material for this manuscript includes the following:

  • Data file S1 (Microsoft Excel format). Individual subject-level data.