AI Article Synopsis

  • Mammalian cardiomyocytes transition from hyperplastic to hypertrophic growth after birth, which is crucial for proper heart function.
  • Researchers studied the role of long non-coding RNAs (lncRNAs) during this transition by analyzing their expression in mouse hearts at different postnatal stages.
  • They found 1,146 lncRNAs with significant expression changes and focused on one particular lncRNA, ENSMUST00000117266, which regulates cardiomyocyte proliferation and is linked to various stress conditions.
  • The findings suggest that certain lncRNAs play key roles in the heart's growth transition after birth.

Article Abstract

Mammalian cardiomyocytes undergo a critical hyperplastic-to-hypertrophic growth transition at early postnatal age, which is important in establishing normal physiological function of postnatal hearts. In the current study, we intended to explore the role of long non-coding (lnc) RNAs in this transitional stage. We analyzed lncRNA expression profiles in mouse hearts at postnatal day (P) 1, P7 and P28 via microarray. We identified 1,146 differentially expressed lncRNAs with more than 2.0-fold change when compared the expression profiles of P1 to P7, P1 to P28, and P7 to P28. The neighboring genes of these differentially expressed lncRNAs were mainly involved in DNA replication-associated biological processes. We were particularly interested in one novel cardiac-enriched lncRNA, ENSMUST00000117266, whose expression was dramatically down-regulated from P1 to P28 and was also sensitive to hypoxia, paraquat, and myocardial infarction. Knockdown ENSMUST00000117266 led to a significant increase of neonatal mouse cardiomyocytes in G0/G1 phase and reduction in G2/M phase, suggesting that ENSMUST00000117266 is involved in regulating cardiomyocyte proliferative activity and is likely associated with hyperplastic-to-hypertrophic growth transition. In conclusion, our data have identified a large group of lncRNAs presented in the early postnatal mouse heart. Some of these lncRNAs may have important functions in cardiac hyperplastic-to-hypertrophic growth transition.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5339910PMC
http://dx.doi.org/10.1038/srep43485DOI Listing

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