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Published on: February 24, 2017
The Synchrony of STARD4-AS1 and H19 Downregulation with Cardiomyocytes Cell Cycle Arrest
Mahshad Shiri1, Fatemeh Movahedi1, Fatemeh Etezadi1
1Department of Stem Cells and Developmental Biology, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran.
Abstract:
Cardiac regeneration is hindered by the permanent cell cycle arrest of cardiomyocytes post-birth, leading to compensatory fibrosis and impaired cardiac function after injury. While the role of cell cycle regulatory proteins is well understood, the impact of long non-coding RNAs (lncRNAs) remains unclear. To address this gap, we reanalyzed public transcriptomic datasets comparing pre- and post-natal ventricular cardiomyocytes. In silico analysis identified differentially expressed lncRNAs, with four candidates selected for further validation. Human embryonic stem cells (hESCs) were differentiated into cardiomyocytes, and their cell cycle status was assessed on Days 10, 20, and 30. The expression of in silico-identified lncRNAs was evaluated in proliferative (Day 10) and non-proliferative (Days 20 and 30) hESC-derived cardiomyocytes, resembling pre- and post-natal ventricular cardiomyocytes. Among the candidates, STARD4-AS1 and H19 showed a permanent downregulation pattern in both in silico and in vitro assays. STARD4-AS1 and H19 lncRNAs might reside in the regulatory network of cardiomyocytes cell cycle arrest and as targets for cardiac regenerative strategies.
Insights
Long non-coding RNAs (lncRNAs) like STARD4-AS1 and H19 are downregulated in adult cardiomyocytes, suggesting they play a role in cell cycle arrest and could be targets for cardiac regeneration therapies.
Area of Science:
- Cardiovascular Biology
- Molecular Biology
- Genomics
Background:
- Cardiomyocyte cell cycle arrest post-birth limits cardiac regeneration and leads to fibrosis after injury.
- The role of long non-coding RNAs (lncRNAs) in this process is not well understood.
- Investigating lncRNAs could reveal new therapeutic targets for heart repair.
Purpose of the Study:
- To identify lncRNAs involved in cardiomyocyte cell cycle arrest.
- To explore the potential of lncRNAs as targets for cardiac regenerative strategies.
Main Methods:
- Reanalysis of public transcriptomic data comparing pre- and post-natal cardiomyocytes.
- In silico identification and validation of differentially expressed lncRNAs.
- In vitro differentiation of human embryonic stem cells (hESCs) into cardiomyocytes.
- Assessment of lncRNA expression in proliferative and non-proliferative cardiomyocytes.
Main Results:
- Four candidate lncRNAs were identified through in silico analysis.
- STARD4-AS1 and H19 lncRNAs were consistently downregulated in non-proliferative (post-natal-like) cardiomyocytes compared to proliferative (pre-natal-like) ones.
- This downregulation pattern was confirmed in both in silico and in vitro studies.
Conclusions:
- STARD4-AS1 and H19 lncRNAs are potential regulators of cardiomyocyte cell cycle arrest.
- These lncRNAs represent promising therapeutic targets for promoting cardiac regeneration.
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