Fig. 4.
M1-Migs promote cardiomyocyte apoptosis through GBP5. (A) Gene ontology analysis (GO) demonstrating the pathways enriched by differentially expressed proteins in M1-Migs/M0-Migs. The apoptotic pathways are highlighted with red rectangles. (B) Western blot analysis of apoptotic proteins in mouse tissues across groups (n = 6). (C) Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) (green) immunostaining for tissue injury analysis across groups. Scale bars = 50 μm (n = 6). (D) Western blot analysis of apoptotic proteins in cardiomyocytes following different treatments (n = 3). (E) Flow cytometry analysis of cell apoptosis rates under different treatments (n = 3). (F) TUNEL (red) immunostaining for cellular injury analysis across groups. Scale bars = 50 μm (n = 6). (G) & H) Western blot comparison of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway-related proteins (P-P65, P65, and inhibitor of kappa B alpha (IκBα)) in myocardial tissues and cardiomyocytes under different treatments (tissues n = 6, cells n = 3). (In vitro: NC group: Cultured in basic medium only, without injury or intervention; MI group: Treated with H2O2-induced injury only, without migrasome intervention; M0-Migs group: Administered M0-Migs intervention after H2O2-induced injury; d. M1-Migs group: Administered M1-Migs intervention after H2O2-induced injury; e. M1-Migs (GBP5-KD) group: Administered M1-Migs (GBP5-KD) intervention after H2O2-induced injury). Results were described as mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001. One-way or two-way ANOVA variance was applied for multivariate analysis. Unpaired t-tests were applied to compare two groups