Fig. 4: EOS activities in cardiac cell death, fibrosis, and cell adhesion.
From: Eosinophils improve cardiac function after myocardial infarction
a, b Immunofluorescent staining detected cleaved caspase 3-positive cardiac myosin heavy chain (MYH)-positive cardiomyocytes (a) and α-SMA-positive fibroblasts (b) in infarct, border, and remote regions of WT mice at 1-month post-MI. Scale: 100 µm, inset: 40 µm. c FACS detection of Annexin V+PI– (propidium iodide) early apoptotic cardiomyocytes after cells were treated with and without H2O2 (100 µM) and EOS lysate (equivalent to 106 EOS/ml) from WT mice. Representative images in a–c are shown to the left. d, e Immunoblot detection of p-Smad2/3, total Smad2/3, and GAPDH in fibroblasts treated with 10 ng/ml TGF-β and different concentrations of EOS lysate (equivalent to 1 × 105, 5 × 105, 1 × 106 EOS per ml) for 30 min. Representative immunoblots are shown to the right. f FACS detection of ICAM-1 and VCAM-1 expression from MHECs after treatment with and without (control) different concentrations of TNF-α (5, 25, and 100 ng/ml). g Adhesion of 5-(and 6)-carboxyfluorescein diacetate succinimidyl ester (CFSE)-labeled neutrophils on TNF-α (100 ng/ml)-treated MHECs after pretreatment with different types of EOS as indicated. Scale: 50 µm. h FACS gating strategy for panel c. The numbers of mice (a, b), the numbers of experiments (c–e, g), and P values are indicated, one-way ANOVA test.
