| First Author | Janssen R | Year | 2013 |
| Journal | Endocrinology | Volume | 154 |
| Issue | 6 | Pages | 1973-8 |
| PubMed ID | 23554452 | Mgi Jnum | J:198195 |
| Mgi Id | MGI:5495846 | Doi | 10.1210/en.2012-2017 |
| Citation | Janssen R, et al. (2013) Cardiac expression of deiodinase type 3 (Dio3) following myocardial infarction is associated with the induction of a pluripotency microRNA signature from the Dlk1-Dio3 genomic region. Endocrinology 154(6):1973-8 |
| abstractText | The adult heart has almost completely lost the proliferative potential of the fetal heart. Instead, loss of cardiomyocytes due to myocardial infarction (MI) leads to a limited, and often insufficient, hypertrophic response of cardiomyocytes in the spared myocardium. This response is still characterized by a partial reexpression of the fetal gene program. Because of the suggested involvement of microRNAs (miRNAs) in cardiac remodeling, we examined the miRNA expression profile of the spared left ventricular myocardium using a MI mouse model. C57Bl/6J mice of either sex were randomly assigned to the sham-operated group or MI group. MI was induced by ligation of the left coronary artery. One week after surgery RNA was isolated from the left ventricle. MiRNA analysis was performed using the Taqman Megaplex rodent array. Unexpectedly, we found a set of 29 up-regulated miRNAs originating from the Dlk1-Dio3 genomic imprinted region, which has been identified as a hallmark of pluripotency and proliferation. This miRNA signature was associated with a 6-fold increase in expression of the deiodinase type 3 gene (Dio3) located in this region. Dio3 is a fetally expressed thyroid hormone-inactivating enzyme associated with cell proliferation, which was shown to be up-regulated in cardiomyocytes creating a local hypothyroid condition in the spared myocardium in this model. These data suggest that a regenerative process is initiated, but not completed, in adult cardiomyocytes after MI. The identified miRNA signature could provide new ways to manipulate the in vivo response of adult cardiomyocytes to stress and to increase the regenerative capacity of the injured myocardium. |
