Figure 1.

miR-1231 is overexpressed in human and rat hearts after MI. A. miR-1231 levels were aberrantly elevated in RNA samples of hearts from both human with MI and from rats subjected to experimental MI. Real-time PCR analysis was used to measure miR-1231 levels. In human samples, MI hearts (n=5) were compared with control non-ischemic hearts (Ctl, n=8); for rat samples, ctl samples as well as three different sections from MI hearts induced for 7 days or 14 days were compared (n=8. NIZ, nonischemic zone; BZ, border zone; IZ, ischemic zone). Data were presented as mean ± s.e.m. and normalized to Ctl. *, P<0.05 compared with Ctl; NS, not significant compared with Ctl. Unpaired Student’s t-test. B. Northern blot analysis of miR-1231 verified the real-time PCR expression data. Northern blot analysis of randomly selected two pairs of human control non-ischemic hearts and MI hearts as indicated (left panel) and rat ctl and three different regions from MI hearts at 14 days post-MI (right panel) showed a consistent increase in miR-1231 in human and rat heart samples in response to MI. 5S rRNA bands stained with ethidium bromide were used as a loading control. C. miR-1231 levels were determined by real-time PCR analysis of RNA samples from neonatal rat cardiac myocytes and fibroblasts cultured under normoxic or hypoxic condition for 48 h. Predominately high expression of miR-1231 in cardiac myocytes compared with fibroblasts was shown, and its expression was even more upregulated in response to hypoxia condition. Comparable amounts of RNA were used in each reaction. *, P<0.05 compared with normoxic cardiac myocytes. NS, not significant compared with normoxic fibroblasts.