PlumX Metrics
Embed PlumX Metrics

HO Induces Myocardial Hypertrophy in H9c2 Cells: A Potential Role of Ube3a

Cardiovascular Toxicology, ISSN: 1559-0259, Vol: 15, Issue: 1, Page: 23-28
2015
  • 15
    Citations
  • 0
    Usage
  • 22
    Captures
  • 0
    Mentions
  • 0
    Social Media
Metric Options:   Counts1 Year3 Year

Metrics Details

Article Description

Myocardial hypertrophy that often leads to eventual heart failure is a leading cause of mortality worldwide. While both apoptosis and cell proliferation have been reported to play an important part in heart failure, its exact triggering mechanism is still unclear. Reports have shown that low concentrations of HO (10–30 µM) can induce myocardial hypertrophy without affecting survival. The ubiquitin ligase Ube3a has been reported to have a close affiliation with Angelman syndrome; but many ubiquitin ligases have been reported in a variety of cardiovascular conditions including myocardial hypertrophy. However, the relationship between Ube3a and myocardial hypertrophy has never been reported in literature. The rat cardiac myoblast cell line H9c2 and primary neonatal cardiomyocytes showed similar hypertrophic responses in vitro. In this report, we utilized HO treatment on H9c2 cells to induce myocardial hypertrophy and determined the relationship between Ube3a and myocardial hypertrophy. Our results showed that 10–20 μM HO can induce myocardial hypertrophy without affecting cell viability and inducing cell apoptosis, while the corresponding transcription and translation levels of Ube3a are significantly increased during the process. Therefore, these findings underline that Ube3a may play an important role in myocardial hypertrophy.

Bibliographic Details

Song, Rui; Zhang, Jie; Zhang, Lijuan; Wang, Guanghua; Wo, Da; Feng, Jian; Li, Xucheng; Li, Jue

Springer Science and Business Media LLC

Biochemistry, Genetics and Molecular Biology; Pharmacology, Toxicology and Pharmaceutics; Medicine

Provide Feedback

Have ideas for a new metric? Would you like to see something else here?Let us know