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Downregulation of Long Noncoding RNA LINC00261 Attenuates Myocardial Infarction through the miR-522-3p/Trinucleotide

Chaoxin Jiang1, Qing Zhao2, Chenlong Wang3

  • 1Department of Clinical Laboratory, Guangdong Provincial Hospital of Integrated Traditional Chinese and Western Medicine, Foshan, Guangdong 528200, China.

Cardiovascular Therapeutics
|July 9, 2021
PubMed
Abstract

Insights

Long noncoding RNA LINC00261 exacerbates myocardial infarction (MI) by downregulating miR-522-3p, leading to increased TNRC6A expression and cardiomyocyte apoptosis. LINC00261 inhibition shows therapeutic potential for MI treatment.

Area of Science:

  • Molecular Biology
  • Cardiovascular Research
  • Genetics

Background:

  • Myocardial infarction (MI) involves cardiac tissue death due to prolonged coronary artery ischemia.
  • Investigating the role of long noncoding RNA (lncRNA) LINC00261 in MI pathogenesis is crucial.
  • Understanding the molecular mechanisms underlying MI can lead to novel therapeutic strategies.

Purpose of the Study:

  • To investigate the expression of lncRNA LINC00261 in myocardial infarction (MI).
  • To elucidate the regulatory network involving LINC00261, miR-522-3p, and TNRC6A in MI.
  • To assess the therapeutic potential of targeting LINC00261 in MI treatment.

Main Methods:

  • Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) to measure LINC00261, miR-522-3p, and TNRC6A expression.
  • Western blotting to detect TNRC6A protein levels.
  • Cell viability and apoptosis assays in cardiomyocytes with manipulated LINC00261 and TNRC6A levels.
  • Double luciferase reporter assays to confirm molecular interactions.

Main Results:

  • LINC00261 and TNRC6A were upregulated, while miR-522-3p was downregulated in MI tissues.
  • LINC00261 knockout enhanced cardiomyocyte viability and reduced apoptosis.
  • LINC00261 directly targets miR-522-3p, which in turn targets TNRC6A, influencing cardiomyocyte apoptosis in MI.

Conclusions:

  • LINC00261 downregulates miR-522-3p in MI cardiomyocytes via direct targeting.
  • TNRC6A is a direct target of miR-522-3p, mediating MI-related effects.
  • LINC00261 presents a potential therapeutic target for myocardial infarction treatment.

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