Figure 8.

miR-24-3p antagomir abrogated the effect of KLF2-EVs on ameliorating myocardial I/R injury. (A) Schematic of myocardial I/R injury model and intravenous infusion of EVs derived from miR-24-3p antagomir or NC antagomir treated HUVECs. (B) Representative images of hearts in Evans blue/TTC staining from mice 3 days following treatment with PBS, NC-EVs or antagomir-EVs. Area-at-risk (AAR): red line; infarct size (IS): white dotted line. Scale bar=5 mm. Quantitative analysis of the percentage AAR and percentage infarct of hearts (n=5). (C) Quantification of infarct area (%) in H.E. staining within the ischemic heart 3 days following operation (n=5). (D) Quantification of scar area in I/R hearts with Masson trichrome staining (n=5). (E) Ejection fraction (EF) and left ventricular end-diastolic diameter (LVDd) of differently treated mice measured by echocardiography 3 days following myocardial I/R injury (n=5). Representative flow cytometry plots showing Ly6C^high Mo/Mø (CD11b+Ly6C^high) and Ly6C^low Mo/Mø (CD11b+Ly6C^low), and quantification of cells within heart tissues (F), in peripheral blood (G) and in spleen (H) 3 days following treatment (n=5). (I) Quantification of CCR2 mRNA of BM with qRT-PCR in sham-operated, I/R, NC-EVs and antagomir-EVs groups (n=5). (J) Representative images of WB and quantification to assess expression of CCR2 within BM in sham-operated, I/R, NC-EVs and antagomir-EVs groups (n=5). Graphs depict mean ± SD. Statistical significance was measured via one-way ANOVA followed by Tukey's multiple comparisons test for multiple groups' comparison and two-way ANOVA followed by Bonferroni's multiple comparisons test for comparison between different groups in different cell subtypes. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, ns= not significant.