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Transcribed ultraconserved region uc.242 is a novel regulator of cardiomyocyte hypertrophy induced by angiotensin II
  1. Ying Gu1,2,
  2. Boyao Zhang3,
  3. Yongchao Yu3,
  4. Fan Yang3,
  5. Yuchen Xiao2,
  6. Weisheng Chen2,
  7. Liping Ma2,
  8. Weizhong Wang4,
  9. Guokun Wang3
  1. 1 Department of Cardiology, Jinling Hospital, Nanjing University School of Medicine, Nanjing, China
  2. 2 Department of Cardiology, Changhai Hospital, Naval Medical University, Shanghai, China
  3. 3 Department of Cardiovascular Surgery, Changhai Hospital, Naval Medical University, Shanghai, China
  4. 4 Laboratory of Marine Biomedicine and Polar Medicine, Naval Medical Center, Naval Medical University, Shanghai, China
  1. Correspondence to Professor Guokun Wang, Shanghai, China; dearwgk{at}; Professor Weizhong Wang; wangwz68{at}


Cardiomyocyte hypertrophy is a response to stress or hormone stimulation and is characterized by an increase of cardiomyocyte size. Abnormal long non-coding RNA (lncRNA) expression profile has been identified in various cardiovascular diseases. Though some lncRNAs had been reported to participate in regulation of cardiac hypertrophy, the universal lncRNA profile of cardiomyocyte hypertrophy had not been established. In the present study, we aimed to identify the differentially expressed lncRNA-mRNA network in angiotensin II-stimulated cardiomyocytes, and screen the potential lncRNAs involved in regulation of cardiomyocyte hypertrophy. The hypertrophic cardiomyocytes were induced by angiotensin II (0.1 μmol/L) for 48 hours. High-throughput microarray analysis combined with quantitative real-time PCR assay were then performed to screen the differentially expressed lncRNAs and mRNAs. A total of 1577 lncRNAs and 496 mRNAs transcripts were identified differentially expressed in hypertrophic cardiomyocytes. Among them, 59 transcribed ultraconserved non-coding RNAs (T-UCRs) were found by evolutionary conservation analysis. Subsequently, the lncRNA-mRNA coexpression network was constructed based on Pearson’s correlation analysis results, including 4 T-UCRs and 215 mRNAs. The results revealed that uc.242 was positively interacted with prohypertrophic genes (Hgf and Tnc). Functional study showed that inhibition of uc.242 dramatically decreased hypertrophic marker expression levels and cardiomyocyte surface area under the condition of angiotensin II stimulation. The expression of Hgf and Tnc was also decreased in cardiomyocytes after silencing of uc.242. Summarily, the present study provided crucial clues to explore therapeutic targets for pathological cardiac hypertrophy.

  • cardiovascular diseases
  • RNA

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  • YG, BZ and YY contributed equally.

  • Contributors GW and LM designed the experiments. YG, BZ and YY performed the experiments. YG, FY and YX analyzed the data. YY and WC performed the statistical analysis. GW and YG wrote the manuscript. WW and GW revised the manuscript.

  • Funding National Natural Science Foundation of China (81470592 and 81800341), and Science of Foundation of Shanghai Municipal Health Planning Commission (201740221).

  • Competing interests None declared.

  • Patient consent for publication Not required.

  • Ethics approval All animal procedures in the present study were approved by the Animal Ethics Committee of Naval Medical University. All experiments were performed in strict compliance with requirements of the Animal Ethics Procedures and Guidelines of China.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Data availability statement Data are available upon reasonable request.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

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