Fig 2: Changes in Lrp1 mRNA and LRP1 protein levels after MI. Frozen myocardial tissue samples (˜ 40 mg) from the remote, peri-infarct and infarct zones were homogenized in TriPure™ Reagent. RNA and protein were isolated as explained in the Materials and Methods. (A) RT-PCR showing Lrp1 mRNA expression levels. Data were processed using a specially designed software program based on the Ct values of each sample and normalized to 18s rRNA, which served as an endogenous control. (B) Representative Western blot analysis results showing LRP1 and troponin T protein expression and bar graphs showing the mean ± S.D. of LRP1 protein bands normalized to troponin T bands. n = 8. *P < 0.05 versus remote; # P < 0.05 versus peri-infarct; **P < 0.01 versus remote; ## P < 0.01 versus peri-infarct; ***P < 0.005 versus remote. (C) Representative immunostaining of heart cross sections showing the temporal evolution of LRP1 levels after MI. LRP1 is shown in red, and cTnI, in green. Cell nuclei were counterstained with DAPI (blue). Scale bars, 20 µm.

Fig 3: rHC matrix increases vascularity and preserves cardiomyocytes post-MI. a Immunohistochemistry analysis and quantification (number/mm2) of capillary and arteriole number in the myocardial scar and border zone after treatment with PBS, rHCI, or rHCIII. CD31, red; a-SMA, green; DAPI, blue (n = 6–7). b Immunohistochemistry analysis and quantification of total area (in mm2) positive for cardiac troponin I (cTnI) staining in the border zone after treatment with PBS, rHCI, or rHCIII. cTnI, red; wheat germ agglutinin, green; DAPI, blue. c Immunohistochemistry analysis and quantification of connexin 43 (Cx43) expression (percent area) in the remote area after treatment with PBS, rHCI, or rHCIII. Cx43, green; cTnI, red; DAPI, blue (n = 6–7). P-values were determined by one-way ANOVA using Holm’s multiple comparison. The data are presented as the mean ± SEM. Source data are provided as a Source Data file. For a–c, n indicates the number of mice per group