Fig. 1 |. Myocardial infarction enhances fatty acid metabolism in hematopoietic stem and progenitor cells.

A, Experimental design. B, Hallmark gene sets significantly (FDR<0.05) enriched in granulocyte monocyte progenitors (GMP) from mice with myocardial infarction (MI). GMP were isolated from the bone marrow of control mice and day 2 after MI (n=3 control, n=3 MI). C, Gene set enrichment analysis showing upregulation of “Hallmark oxidative phosphorylation”, “Hallmark fatty acid metabolism” and “C2 Reactome respiratory electron transport” in GMP isolated from mice with MI. D, Real-time changes in the oxygen consumption rate (OCR) of GMP sorted from control mice compared to day 3 after MI (n=5 control, n=5 MI, two independent experiments), assessed by Seahorse assay. E, Quantification of basal OCR, spare respiration capacity (SRC), extracellular acidification rate (ECAR) and OCR/ECAR ratio of GMP sorted from control mice versus day 3 after MI (n=5 control, n=5 MI, two-tailed Welch’s t test, two independent experiments). F, Abundance of citrate, percentage of ¹³C₂ labelled citrate, and amount of total ¹³C₂ citrate as measured by mass spectrometry in 300,000 GMP isolated from control and day 3 post-MI mice that were injected with ¹³C₁₆ palmitate (n=8 mice per group, two-tailed Mann-Whitney test, two independent experiments). G, Flow cytometry gating for hematopoietic stem and progenitor cells (HSPC) in mice and histogram of MitoTracker^™ Green FM intensity in GMP from controls and mice on day 3 after MI. H, Mean fluorescence intensity (MFI) of MitoTracker^™ Green staining in control mice versus day 3 after MI (n=5 control, n=6 MI, two-tailed Welch’s t test). Data are displayed as mean±SEM.