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. 2008 Aug 22;105(35):13027–13032. doi: 10.1073/pnas.0805038105

Fig. 1.

Fig. 1.

MiRNA profiling in response to MI. (A) Masson Trichrome staining of mouse heart sections shows early scar formation 3 days after MI, with myocyte hypertrophy, loss of myocytes, and collagen deposition. Fourteen days after MI, there is a thin stretched infarct that results in cardiac hypertrophy and interstitial fibrosis in the border zone of the infarcted region. I, infarct; BZ, borderzone; R, remote myocardium. (Lower) Higher magnification of the borderzone regions of the infarcted hearts and the comparable level of the sham operated heart. (Scale bars: Upper, 2 mm; Lower, 20 μm). (B) Microarray analysis reveals miRNAs are dynamically regulated in response to MI. Even after initial infarct healing, 14 days after MI, 11 miRs are overlappingly up-regulated, whereas 15 miRs are down-regulated. The number of miRNAs regulated ≥2-fold in each category is shown. (C) Real-time PCR analysis confirms the regulation of specific miRNAs in response to MI compared with sham operated animals (n = 3–4. S, sham; BZ, borderzone; R, remote. *, P < 0.05 compared with sham operated animals). (D) Real-time PCR analysis shows the regulation of miRNAs in human heart samples in response to MI compared with nonfailing hearts (n = 5–6, NF = nonfailing, MI = myocardial infarction). *, P < 0.05 compared with nonfailing hearts. (E) Northern blot analysis of three nonfailing human hearts and five human hearts after MI indicates a consistent increase in miR-21 in the borderzone of human heart samples in response to MI.