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The lncRNA ADAMTS9-AS1/miR-185-5p/KAT7 ceRNA network inhibits cardiomyocyte hypertrophy in hypertrophic obstructive

Bangrong Song1, Wei Li1, Xiaoyu Xu1

  • 1Capital Medical University.

Biomedical Research (Tokyo, Japan)
|May 31, 2023
PubMed

Insights

Long non-coding RNA ADAMTS9-AS1 (lncRNA ADAMTS9-AS1) is downregulated in hypertrophic obstructive cardiomyopathy (HOCM). Overexpression of lncRNA ADAMTS9-AS1 inhibits HOCM-induced cardiomyocyte hypertrophy by regulating the miR-185-5p/KAT7 axis.

Area of Science:

  • Cardiovascular Biology
  • Molecular Genetics
  • Epigenetics

Background:

  • Hypertrophic obstructive cardiomyopathy (HOCM) is a significant inherited cardiac condition.
  • Understanding the molecular mechanisms underlying HOCM-induced cardiomyocyte hypertrophy is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the role of long non-coding RNA ADAMTS9 antisense RNA 1 (lncRNA ADAMTS9-AS1) in HOCM-associated cardiomyocyte hypertrophy.
  • To elucidate the regulatory pathway involving lncRNA ADAMTS9-AS1, miR-185-5p, and KAT7 in HOCM.

Main Methods:

  • Quantitative real-time PCR (qRT-PCR) and Western blot assays were used to measure gene and protein expression levels.
  • Cellular assays, including Texas Red-Phalloidin staining, assessed cardiomyocyte surface area.
  • RNA pull-down and dual-luciferase assays were employed to validate molecular interactions.

Main Results:

  • lncRNA ADAMTS9-AS1 expression was found to be downregulated in HOCM patient serum and in isoproterenol (ISO)-treated cardiomyocytes.
  • Overexpression of lncRNA ADAMTS9-AS1 attenuated ISO-induced cardiomyocyte hypertrophy and reduced levels of cardiac hypertrophy markers (BNP, ANP).
  • lncRNA ADAMTS9-AS1 directly targets and inhibits miR-185-5p, which in turn targets and inhibits KAT7, thereby modulating cardiomyocyte hypertrophy.

Conclusions:

  • lncRNA ADAMTS9-AS1 plays a protective role against HOCM-induced cardiomyocyte hypertrophy.
  • The mechanism involves lncRNA ADAMTS9-AS1 acting as a molecular sponge for miR-185-5p, leading to the upregulation of KAT7.
  • This regulatory axis presents a potential therapeutic target for HOCM.

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