ArticleIn vitro cellular & developmental biology. Animal2019
LncRNA TUG1 contributes to cardiac hypertrophy via regulating miR-29b-3p.
Article in In vitro cellular & developmental biology. Animal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Posttranscriptional Regulation by Proteins and Noncoding RNAs.Advances in experimental medicine and biology · 2024Article
- Mesenchymal stem cells-derived extracellular vesicle-incorporated H19 attenuates cardiac remodeling in rats with heart failure.The Kaohsiung journal of medical sciences · 2024Article
- SLC26A4-AS1 Aggravates AngII-induced Cardiac Hypertrophy by Enhancing SLC26A4 Expression.Arquivos brasileiros de cardiologia · 2023Article
- Review
- Emerging roles of the RNA modifications N6-methyladenosine and adenosine-to-inosine in cardiovascular diseases.Molecular therapy. Nucleic acids · 2022Review
- lncRNA NBR2 attenuates angiotensin II-induced myocardial hypertrophy through repressing ER stress via activating LKB1/AMPK/Sirt1 pathway.Bioengineered · 2022Article
- TUG1 knockdown suppresses cardiac fibrosis after myocardial infarction.Mammalian genome : official journal of the International Mammalian Genome Society · 2021Article
- Differentially expressed TUG1 and miR-145-5p indicate different severity of chronic heart failure and predict 2-year survival prognosis.Experimental and therapeutic medicine · 2021Article
- LncRNA TUG1 aggravates cardiomyocyte apoptosis and myocardial ischemia/reperfusion injury.Histology and histopathology · 2021Article
- Reconnoitering the Role of Long-Noncoding RNAs in Hypertrophic Cardiomyopathy: A Descriptive Review.International journal of molecular sciences · 2021Review
- The function of LncRNA-H19 in cardiac hypertrophy.Cell & bioscience · 2021Review
- Serum NT-proBNP and TUG1 as novel biomarkers for elderly hypertensive patients with heart failure with preserved ejection fraction.Experimental and therapeutic medicine · 2021Article
- MiR-29b-3p aggravates cardiac hypoxia/reoxygenation injury via targeting PTX3.Cytotechnology · 2021Article
- LncRNA TUG1 Regulates Proliferation of Cardiac FibroblastFrontiers in cardiovascular medicine · 2021Article
- Knockdown of TUG1 rescues cardiomyocyte hypertrophy through targeting the miR-497/MEF2C axis.Open life sciences · 2021Article
- A miRNA's insight into the regenerating heart: a concise descriptive analysis.Heart failure reviews · 2020Review
- LDNFSGB: prediction of long non-coding rna and disease association using network feature similarity and gradient boosting.BMC bioinformatics · 2020Article
- SP1-induced SNHG14 aggravates hypertrophic response in in vitro model of cardiac hypertrophy via up-regulation of PCDH17.Journal of cellular and molecular medicine · 2020Article
- Long Noncoding RNA FTX Reduces Hypertrophy of Neonatal Mouse Cardiac Myocytes and Regulates the PTEN/PI3K/Akt Signaling Pathway by Sponging MicroRNA-22.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac hypertrophy with maladjusted cardiac remodeling is the leading cause of heart failure. In the past decades, long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) have been proved to exert multiple functions in cellular biological behaviors; however, their role in cardiac hypertrophy remains largely unclear. Presently, we first obtained hypertrophic H9c2 cells by treating with angiotensin II (Ang II) and uncovered upregulation of lncRNA taurine upregulated gene 1 (TUG1) in such H9c2 cells. Then, we demonstrated that silencing TUG1 attenuated Ang II-induced cardiac hypertrophy. Besides, a strong interactivity of TUG1 with miR-29b-3p at the putative sites was validated, suggesting that TUG1 was an endogenous sponge of miR-29b-3p in H9c2 cells. Additionally, the expression of miR-29b-3p was strikingly reduced by TUG1 upregulation and also inhibited under Ang II treatment, whereas it was restored after silencing TUG1 in hypertrophic cells. Also, we proved miR-29b-3p as a negative regulator in cardiac hypertrophy. Finally, miR-29b-3p inhibition abolished the anti-hypertrophy effect of TUG1 depletion in Ang II-treated H9c2 cells. Collectively, our findings confirmed that TUG1 functioned as a positive modulator of cardiac hypertrophy via sponging miR-29b-3p, indicating that TUG1 might serve as a potential target for the treatment of cardiac hypertrophy and even heart failure.
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