Figure 3: CTGF mAb Protects Against Post-MI LV Hypertrophy and Fibrosis (Study II)

Mice were subjected to MI and 1 week after surgery randomly divided to receive IgG vehicle or CTGF mAb for 6 weeks. (A) Analysis for heart weight to body weight (HW/BW) ratio, LV mass, left atrial end-diastolic area (LAA;d), and EF. (B) Analysis of cardiomyocyte cross-sectional area from Masson trichrome−stained LV sections. (C) Analysis of mean capillary cross-sectional size and the number of capillaries per cardiomyocyte in the nonischemic myocardium from CD31 staining, (D) Analysis of interstitial fibrosis from picrosirius red−stained LV sections under polarized light. Scale bar: 50 μm. (A to D) Data are presented as mean ± SD; number of animals was sham (n = 5), IgG (n = 7), and CTGF mAb (n = 8). *p < 0.05; **p < 0.01; ***p < 0.001. (E) Hierarchical clustering of RNAseq data for transcripts that were altered by MI and at least partially normalized by CTGF mAb, indicating that many of these genes are regulated by transforming growth factor-β1 (TGF-β1), tumor necrosis factor (TNF)-α, or interleukin (IL)-1β. Red highlights indicate genes associated with various fibrotic disorders. (F) Hierarchical clustering of RNAseq data showing transcripts whose expression was increased in hearts of mice treated with CTGF mAb. Known cardiac development and/or repair related genes are highlighted (red). (E and F) Number of animals was sham (n = 3), IgG (n = 5), and CTGF mAb (n = 5). Abbreviations as in Figures 1 and 2.