Fig. 7

Mdka-Lrp1 signaling promotes col12a1a+ fibroblast activation, collagenous scar turnover, re-vascularization, and myocardial repair (A and B) Macrophage (mCherry+) expression of mdka, detected by HCR-FISH, in sham-operated and cryoinjured csf1ra:Gal4; UAS:NTR-mCherry and csf1ra:Gal4; UAS:NTR-mCherry; UAS:adra1-3i-T2A-CFP heart section at 7 dpi (A), and quantified as numbers of mdka+mCherry+ cells per ventricular area (B). (C–F) Type-I collagen deposition (C) and collagen degradation (E) in control and Lrpap1-treated explanted heart sections, measured as percentages of Col1 (D) and CHP (F) area per injured ventricular area at 7 dpi. (G and H) Proliferating cardiomyocytes (white circles), marked by immunofluorescent staining of 7 dpi control and Lrpap1-treated explanted heart sections with antibodies against PCNA and Mef2 (G), and measured as percentages of total cardiomyocytes within the measurement area (H). (I–K) Blood and lymphatic vessel growth within the lesion of 7 dpi control and Lrpap1-treated heart explants detected by CD31 immunofluorescence and lyve1 HCR-FISH, respectively (I), and measured as a percentage of vessel area (%) and number of endothelial cells over total area measured (J and K). Lrp1aa-expressing col12a1a+ fibroblast subset in control and Lrpap1-treated heart explants, marked by immunofluorescence of a-SMA and HCR-FISH of col12a1a and lrp1aa (L), and quantified as percentages of a-SMA+col12a1a+lrp1aa+ cells per total a-SMA+col12a1a+ fibroblasts (M). All scale bars: 20 μm. DAPI labeled all nuclei. White dashed lines demarcate injured areas. Data are displayed as mean ± SEM and data points of individual animals. n denotes number of animals measured for each group. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001; n.s. not significant, two-tailed t test.