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. Author manuscript; available in PMC: 2022 Mar 2.
Published in final edited form as: J Am Coll Cardiol. 2021 Mar 2;77(8):1073–1088. doi: 10.1016/j.jacc.2020.12.060

Figure 3. Non-mitochondrial cargo in D15 M-EVs restored bioenergetics through activation of PGC-1α-mediated mitochondrial biogenesis in the recipient iCMs.

Figure 3.

A. PGC-1α and ERRγ mRNA, normalized to U6, were upregulated in D15 Ld-EVs (n=4/group). *P<0.05 by an unpaired t-test. B. Quantitative gene expression in iCMs, normalized to ACTB shown as fold change relative to normoxic iCMs (n=4–5/group). C. Seahorse extracellular-flux assays measuring oxygen-consumption rate (OCR) (n=5–6/group). *P<0.01, **P<0.001 and ***P<0.0001 by a one-way ANOVA followed by Tukey’s test. ATP5A1=ATP synthase F1 α-subunit; COX6A1=cytochrome c oxidase subunit-6A1; Cs=citrate synthase; CYC1=cytochrome c1; ERRγ=estrogen-related receptor γ; FCCP=carbonyl cyanide-4-(trifluoromethoxy)phenylhydrazone; NRF1=Nuclear respiratory factor-1; NDUFA1=NADH dehydrogenase-1α subcomplex subunit-1; PGC-1α=peroxisome proliferator-activated receptor γ coactivator 1α; PKM=pyruvate kinase M1/2; SDHA=succinate dehydrogenase complex flavoprotein subunit-A; TFAM=mitochondrial transcription factor-A.