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Related Experiment Video

Updated: Feb 11, 2026

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H19 Induces Abdominal Aortic Aneurysm Development and Progression.

Daniel Y Li1, Albert Busch1, Hong Jin2

  • 1Department of Vascular and Endovascular Surgery, Klinikum rechts der Isar (D.Y.L., A. Busch, J.P., S.L., H.-H.E., L.M.), Technical University Munich, and German Center for Cardiovascular Research (DZHK), partner site Munich, Germany.

Circulation
|April 20, 2018
PubMed
Summary

The long noncoding RNA H19 regulates smooth muscle cell survival in abdominal aortic aneurysm development. Inhibiting H19 may offer a new therapeutic strategy for aortic aneurysm disease.

Keywords:
abdominal aortic aneurysmlong noncoding RNAmolecular medicinesmooth muscle cellstranslations

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Area of Science:

  • Molecular Biology
  • Genetics
  • Cardiovascular Research

Background:

  • Long noncoding RNAs (lncRNAs) are key regulators in biological processes and diseases.
  • Abdominal aortic aneurysm (AAA) development involves complex molecular mechanisms.
  • Identifying novel lncRNAs in AAA pathogenesis is crucial for therapeutic development.

Purpose of the Study:

  • To identify and functionally characterize lncRNAs involved in abdominal aortic aneurysm (AAA) development.
  • To investigate the role of the lncRNA H19 in AAA pathogenesis.
  • To explore H19 as a potential therapeutic target for AAA.

Main Methods:

  • RNA transcript expression profiling in two murine AAA models (Angiotensin II infusion and porcine pancreatic elastase instillation).
  • Quantitative reverse transcription-polymerase chain reaction and in situ hybridization to confirm H19 expression.
  • In vivo and in vitro experiments using antisense oligonucleotides (LNA-GapmeRs) for H19 knock-down and overexpression in smooth muscle cells (SMCs).
  • Analysis of H19's downstream effectors, including hypoxia-inducible factor 1α (HIF-1α) and p53.

Main Results:

  • The lncRNA H19 was significantly upregulated in both murine AAA models.
  • Experimental knock-down of H19 reduced aneurysm growth and SMC apoptosis in vivo.
  • H19 overexpression increased SMC apoptosis in vitro, independent of miR-675.
  • H19 interacts with HIF-1α in the cytoplasm, leading to p53 stabilization and increased SMC apoptosis.
  • H19 promotes HIF-1α transcription by recruiting specificity protein 1.

Conclusions:

  • The lncRNA H19 is a novel regulator of SMC survival and apoptosis in abdominal aortic aneurysm development and progression.
  • H19 plays a critical role in the pathogenesis of AAA.
  • Inhibition of H19 represents a potential novel molecular therapeutic strategy for aortic aneurysm disease.