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Circ-TLR4 promotes cardiac hypertrophy through recruiting FUS to stabilize TLR4 mRNA

Chao Li1, Jingwen Wang2, Jun Feng3

  • 1Department of Cardiology, Hefei Hospital Affiliated to Medical University of Anhui (the Second People's Hospital of Hefei), Hefei, 230011, Anhui, China.

Journal of Interventional Cardiac Electrophysiology : an International Journal of Arrhythmias and Pacing
|May 13, 2022
PubMed

Insights

Circular RNA of Toll-like receptor 4 (circ-TLR4) promotes cardiac hypertrophy by stabilizing its messenger RNA. This finding reveals a novel mechanism in cardiovascular disease development.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • RNA Biology

Background:

  • Cardiac hypertrophy is a compensatory response to stress, but its dysregulation contributes to cardiovascular disease.
  • Circular RNAs (circRNAs) play roles in cardiovascular diseases, including cardiac hypertrophy.
  • Toll-like receptor 4 (TLR4) is implicated in inflammation and cardiac hypertrophy, but its circular isoforms are unstudied.

Purpose of the Study:

  • To investigate the role of circ-TLR4 in cardiac hypertrophy.
  • To elucidate the molecular mechanism by which circ-TLR4 influences cardiac hypertrophy.

Main Methods:

  • RT-qPCR to measure circ-TLR4 and TLR4 expression in cardiomyocytes.
  • Immunofluorescence and western blot to assess cardiac hypertrophy markers (cell surface area, ANF, BNP, β-MHC).
  • RIP assay to confirm the interaction between circ-TLR4 and TLR4.

Main Results:

  • Circ-TLR4 and TLR4 expression increased in cardiac hypertrophy models.
  • Knockdown of circ-TLR4 reduced angiotensin II-induced hypertrophy.
  • Circ-TLR4 stabilizes TLR4 mRNA by recruiting FUS.
  • TLR4 overexpression reversed the effects of circ-TLR4 silencing.

Conclusions:

  • Circ-TLR4 promotes cardiac hypertrophy.
  • The mechanism involves FUS-mediated stabilization of TLR4 mRNA.
  • Circ-TLR4 is a potential therapeutic target for cardiac hypertrophy.
Abstract

Keywords:
Cardiac hypertrophyCirc-TLR4FUSTLR4

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