Fig 1: CDMG1 administration increases newly formed CMs and reduces fibrotic scar tissue in infarcted mouse hearts. (A) Schematic of CDMG1 treatment and EdU pulse experiments during MI. EdU was intraperitoneally injected (500 µg/animal) every 2 days post-MI. (B) Diagram of sections in post-MI hearts. IZ, infarct zone; RZ, remote zone; BZ, boarder zone. (C–F) Immunofluorescence analyses showing EdU+TPM+ CMs (arrows) in the border zone in CDMG1-treated hearts and DMSO-treated hearts. Red: EdU; green: TPM1. (G–J) Immunofluorescence images revealing an increase of Ph3+TPM+ cells in the border zone in post-MI hearts. Red: Ph3; green: TPM1. (K, L) Quantitative analyses of CM proliferation activity in CDMG1-treated MI mice. Data are presented as mean ± SEM; Student’s t-test: P represents statistical values in MI + CDMG1 group (n = 3, four sections per animal) compared to MI + DMSO group (n = 3, four sections per animal). ns, not significant. For EdU analysis, 4370 cells (infarct border zone) and 4610 cells (remote zone) in MI + DMSO group and 4361 cells (infarct border zone) and 4406 cells (remote zone) in MI + CDMG1 group were examined. For Ph3 analysis, 9244 cells (infarct border zone) and 8887 cells (remote zone) in MI + DMSO group and 8942 cells (infarct border zone) and 9142 cells (remote zone) in MI + CDMG1 group were examined. (M) The diagram of five sequential transversal sections of hearts (L1–L5, 3 µm thick) at 28-day post-MI. X: MI site. (N) Representative images of Masson trichrome staining of L1–L5 sections. Collagen-rich area (scar) stained in blue and healthy myocardium stained in red. (O) Fibrotic length percentage was calculated by dividing the midline length of total LV wall with the length of the infarcted LV wall. Data are presented as mean ± SEM; Student’s t-test: P represents the statistic value of MI + CDMG1 group (n = 4) versus MI + DMSO group (n = 4). Scale bar, 40 µm (C–J).