Fig. 1.

Silencing Malat1 in CMECs aggravated myocardial infarction (MI) and microvascular dysfunction. Time course of the relative expression of Malat1 in cardiac tissues and CMECs in the infarct border zone and remote areas after MI (A, B). One-week overall survival curve (C). Analysis of brain natriuretic peptide (BNP) levels in serum (D). The M-mode of echocardiography images and the data on left ventricular end-diastolic diameter (LVEDD), ejection fraction (EF) and fractional shortening (FS) for each group (E). Heart weight to body weight ratio (HW/BW) for each group (F). HE staining, Masson staining and quantification of cardiac fibrosis (G, H). Analyses of cardiac troponin T (cTnT) concentration and lactate dehydrogenase (LDH) activity in serum (I, J). Microvascular perfusion of the border zone was indicated by the ratio of lectin-perfused vessels (green) to CD31-positive ECs (red) (K). Immunofluorescence staining for eNOS (L). Nitric oxide (NO) content in the border zone of each group (M). Immunofluorescence staining for VEGFR2 (N). eNOS expression and phosphorylation at Ser¹¹⁷⁷ in the border zone were analysed by Western blotting (O). VEGFR2 expression and phosphorylation at Tyr¹¹⁷⁵ in the border zone were analysed by Western blotting (P). *p < 0.05 compared with the sham group, #p < 0.05 compared with the MI + Scr-shRNA group. n = 6 in each group.