Identification of Circular RNAs Regulating Cardiomyocyte Proliferation in Neonatal Pig Hearts
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ABSTRACT:
PROVIDER: PRJNA1122191 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29350100_1.fastq.gz | Fastqsanger.gz | |||
| SRR29350100_2.fastq.gz | Fastqsanger.gz | |||
| SRR29350101_1.fastq.gz | Fastqsanger.gz | |||
| SRR29350101_2.fastq.gz | Fastqsanger.gz | |||
| SRR29350102_1.fastq.gz | Fastqsanger.gz |
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Project description:Little is known about the expression patterns and functions of circular RNAs (circRNAs) in the heart of large mammals. In this study, we examined the expression profiles of circRNAs, microRNAs (miRNAs), and messenger RNAs (mRNAs) in neonatal pig hearts. Pig heart samples collected on postnatal days 1 (P1), 3 (P3), 7 (P7) and 28 (P28) were sent for total RNA sequencing. Our data revealed a total of 7000 circRNAs in the 24 pig hearts. Pathway enrichment analysis of hallmark gene sets demonstrated that differentially expressed circRNAs are engaged in different pathways. The most significant difference was observed between P1 and the other three groups (P3, P7 and P28) in pathways related to cell cycle and muscle development. Out of the ten circRNAs that were validated through real-time quantitative polymerase chain reaction (qRT-PCR) to confirm their expression, six exhibited significant effects on cell cycle activity in human induced pluripotent stem cells-derived cardiomyocytes (hiPSC-CMs) following small interfering RNA-mediated knockdown. The circRNA-miRNA-mRNA networks were constructed to understand the potential mechanisms of circRNAs in the heart. In conclusion, our study provided a dataset for exploring the roles of circRNAs in pig hearts. In addition, we identified several circRNAs that regulate cardiomyocyte cell cycle.
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Project description:In mammals, the neonatal heart regenerates within a short time after birth, but adults lack this ability. We have shown that metabolic reprogramming is critical for cardiomyocyte proliferation in the neonatal heart. Herein, we revealed that cardiac metabolic reprogramming could be regulated by altering global protein lactylation. 4D label-free proteomics and Kla omics were performed in postnatal Day 1 (P1), 5 (P5), and 7 (P7) mouse hearts, 2297 Kla sites from 980 proteins were identified, and 1262 Kla sites from 409 proteins were quantified. Functional clustering analysis of proteins with altered Kla sites revealed that the proteins were mainly involved in metabolic processes. The Kla levels in several fatty acid oxidation-related proteins showed high expression at P5, while glycolysis and cell cycle-related proteins were sustainedly decreased from P1-P7. Furthermore, we verified the Kla levels of several differentially modified proteins, including ACAT1, ACADL, PKM and NPM1, by coimmunoprecipitation and Western blotting. Overall, we reported the first comprehensive Kla map in the neonatal mouse heart, which will aid in understanding the regulatory network of metabolic reprogramming and cardiac regeneration.
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Project description:Significance Heart disease accounts for 1 in 4 deaths in the United States annually, making it one of the leading causes of death and related morbidity resents a significant economic burden. Mammalian cardiomyocytes are terminally differentiated with low turnover rate, insufficient to repopulate myocardium after heart attack caused by myocardial infarction (MI). As such, there is an urgent need for the development of non-invasive, effective, and efficient therapeutic approaches for treating MI. One strategy is to promote proliferation in mature cardiomyocytes, inspired by the observation of a transient regenerative window in neonatal mouse cardiomyocytes. During postnatal development, it is believed that cardiomyocytes exit cell cycle in response to high oxygen environment and a metabolic shift to oxidative phosphorylation. Strategies to lower oxidative stress in neonatal mouse hearts to prolong regenerative time window have been reported. While many studies have focused on mitigating injury-related ROS, it is not clear whether the developmental ROS increase in neonatal cardiomyocytes plays a role during postnatal myocardial maturation and establishment of injury response. The following study details the crucial role of neonatal ROS as signaling molecules in cardiomyocyte injury response after MI.
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