Science Advances

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  • fig. S1. hMSCs differentiate into adipogenic and osteogenic lineages.
  • fig. S2. GPMVs prepared from hMSCs.
  • fig. S3. Validation of GPMVs as PM-enriched preparations.
  • fig. S4. Lipidomic differentiation of CMs.
  • fig. S5. DHA-induced remodeling of the MSC lipidome.
  • fig. S6. Distribution of lipids containing ω-6 PUFAs.
  • fig. S7. Supplementation with DHA increases the order difference between ordered and disordered domains in GPMVs.
  • fig. S8. DHA supplementation does not enhance adipogenic differentiation of hMSCs.
  • fig. S9. DCA treatment phenocopies membrane effects of DHA and enhances osteogenic differentiation.
  • fig. S10. Correlation between DHA- and osteogenic-induced effects on protein expression.
  • fig. S11. DCA treatment enhances Akt signaling.
  • fig. S12. Uncropped representative Western blots.
  • fig. S13. Effects of DHA and MZ on membrane organization and Akt activity in BHKs.
  • fig. S14. Row identifiers for Fig. 4D.
  • table S1. Variables and principal component correlation coefficients (loadings) for PCA of CM and PM lipids isolated from adipogenic, osteogenic, and undifferentiated cells (fig. S3).
  • table S2. Variables and principal component correlation coefficients (loadings) for PCA of PM lipids isolated from adipogenic, osteogenic, and undifferentiated cells (Fig. 1I).
  • table S3. Variables and principal component correlation coefficients (loadings) for PCA of CM lipids isolated from adipogenic, osteogenic, and undifferentiated cells treated with DHA (Fig. 2L).
  • table S4. PPAR target genes are induced by adipogenesis but not induced or enhanced by DHA supplementation.

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