| First Author | Patrick DM | Year | 2010 |
| Journal | J Clin Invest | Volume | 120 |
| Issue | 11 | Pages | 3912-6 |
| PubMed ID | 20978354 | Mgi Jnum | J:166911 |
| Mgi Id | MGI:4850192 | Doi | 10.1172/JCI43604 |
| Citation | Patrick DM, et al. (2010) Stress-dependent cardiac remodeling occurs in the absence of microRNA-21 in mice. J Clin Invest 120(11):3912-6 |
| abstractText | MicroRNAs inhibit mRNA translation or promote mRNA degradation by binding complementary sequences in 3' untranslated regions of target mRNAs. MicroRNA-21 (miR-21) is upregulated in response to cardiac stress, and its inhibition by a cholesterol-modified antagomir has been reported to prevent cardiac hypertrophy and fibrosis in rodents in response to pressure overload. In contrast, we have shown here that miR-21-null mice are normal and, in response to a variety of cardiac stresses, display cardiac hypertrophy, fibrosis, upregulation of stress-responsive cardiac genes, and loss of cardiac contractility comparable to wild-type littermates. Similarly, inhibition of miR-21 through intravenous delivery of a locked nucleic acid-modified (LNA-modified) antimiR oligonucleotide also failed to block the remodeling response of the heart to stress. We therefore conclude that miR-21 is not essential for pathological cardiac remodeling. |
