MicroRNA-208a Dysregulates Apoptosis Genes Expression and Promotes Cardiomyocyte Apoptosis during Ischemia and Its Silencing Improves Cardiac Function after Myocardial Infarction

Figure 5

miR-208a silencing attenuates cardiomyocyte hypertrophy and fibrosis and improves cardiac function at 28 days after MI (, ). (a) Representative images of hematoxylin and eosin staining indicate a decrease in cardiomyocyte size in antagomir treated mice at 28 days after MI. Scale bar = 40 µm. (b) Graph comparing mean cardiomyocyte sizes at 28 days after MI. Antagomir treatment decreased the mean cardiomyocyte size compared to controls ( per group). (c) Graph showing percentage fibrosis in the noninfarcted area. Antagomir treatment decreased fibrosis in the noninfarcted area compared to controls at 28 days after MI ( per group). (d) Representative images showing miR-208a antagomir decreased fibrosis in the noninfarcted area at 28 days after MI. (e) Bar graph of peri-infarct fibrosis quantification shows reduction in peri-infarct fibrosis in antagomir treatment group at 28 days after MI ( per group). (f) miR-208a silencing improved cardiac function as measured by fractional shortening at 28 days after MI ( per group). (g) Representative echocardiography images showing improved wall motion in antagomir treated group compared to control at day 28 after MI.

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