AI Article Synopsis
- - Myeloid cell leukemia 1 (Mcl1) is important in the heart because it helps prevent inflammation and fibrosis, which can lead to heart failure.
- - Angiotensin II (Ang II) treatment reduces Mcl1 levels in both adult and neonatal heart tissues, suggesting a link between Mcl1 expression and heart stress.
- - The 3'-untranslated regions (3'-UTR) of mRNA play a protective role by preventing heart cell death caused by Ang II, potentially paving the way for new gene therapy approaches focused on mRNA regulation.
Article Abstract
Myeloid cell leukemia 1 (Mcl1), an abundant protein in the myocardium, plays an essential role in fibrosis and anti-inflammation in cardiomyocytes to prevent heart failure. However, whether 3'-untranslated regions (3'-UTR) has the cardio-protecting function remains unclear. Down-regulation of Mcl1 was observed in adult mice heart tissues after Angiotensin II (Ang II) treatment. Consistent with results, the reduction of Mcl1 expression was identified in Ang II-treated neonatal cardiomyocytes. Mechanistically, 3'-UTR prevented Ang II-induced cardiac apoptosis via up-regulation of Mcl1 and an angiogenic factor with a G-patch domain and a forkhead-associated domain 1 (Aggf1), which plays cardiac-protective role. Our work broadens the scope of gene therapy targets and provides a new insight into gene therapy strategies involving mRNAs' 3'-UTRs application.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7813760 | PMC |
| http://dx.doi.org/10.3389/fcell.2020.593955 | DOI Listing |
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