Fig. 2.

M1-Migs exacerbate cardiomyocyte and tissue injuries. (A) Schematic illustration of mouse model construction by ligating the left anterior descending (LAD) artery, followed by the intramyocardial injection of migrasomes into the infarct zone (created with BioRender.com). (B) Comparison of the survival rates of MI mice after intramyocardial injection of M0-Migs or M1-Migs (normal control (NC) group n = 6, MI group n = 20, M0-Migs group n = 15, M1-Migs group n = 16). (C) Echocardiography analysis 28 days post-infarction. Comparison of left ventricular ejection fraction (LVEF), fractional shortening (LVFS), and end-diastolic volume (LVEDV) among groups (n = 6). (D) Masson’s trichrome staining of cardiac tissue sections for infarct area comparison. Scale bars = 0.500 mm (n = 6). (E) Hematoxylin and eosin (HE) staining to detect myocardial tissue injury in each group. Scale bars = 50 μm (n = 6). (F) Triphenyltetrazolium chloride (TTC) staining demonstrating a significantly larger MI area in the M1-Migs group than that in the M0-Migs and MI groups. Scale bars = 1 cm (n = 6). (G) Cell counting kit-8 (CCK-8) assay for viability of HL-1 cells under different treatments. The stimulation concentration of migrasomes was 100 µg/ml (n = 4). (H) Calcein/propidium iodide (PI) cell viability and toxicity assay for HL-1 cells under different treatments. Scale bars = 100 μm (n = 3). Results are described as mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001. One-way or two-way ANOVA was applied for multivariate analysis, and unpaired t-tests were applied for comparison between the two groups