Promoting role of circ-Jarid2/miR-129-5p/Celf1 axis in cardiac hypertrophy

Area of Science:

• Cardiovascular Biology
• Molecular Cardiology
• Epigenetics

Background:

• Cardiac hypertrophy, a significant risk factor for heart failure, is linked to the dysregulation of RNA-binding proteins like Celf1.
• Understanding the upstream regulatory mechanisms of Celf1 in cardiac hypertrophy is crucial for developing effective treatments.

Purpose of the Study:

• To elucidate the precise function of Celf1 in cardiac hypertrophy.
• To investigate the regulatory network involving Celf1 in the context of cardiac hypertrophy.

Main Methods:

• Angiotensin-II (Ang-II) treatment to induce hypertrophic phenotypes in H9C2 and cardiomyocyte (MCM) cell lines.
• Immunofluorescence assays to quantify cardiomyocyte surface area.
• Quantitative reverse transcription PCR (qRT-PCR) and Western blot assays to analyze gene and protein expression levels.

Main Results:

• Celf1 expression increased with elevated Ang-II concentrations, and inhibiting Celf1 alleviated Ang-II-induced cardiac hypertrophy.
• circ-Jarid2 directly targets miR-129-5p, and miR-129-5p targets Celf1.
• circ-Jarid2 promotes cardiac hypertrophy, while miR-129-5p exhibits suppressive effects; the circ-Jarid2/miR-129-5p/Celf1 axis was confirmed to aggravate cardiac hypertrophy in vitro and in vivo.

Conclusions:

• The circ-Jarid2/miR-129-5p/Celf1 axis plays a critical role in aggravating cardiac hypertrophy.
• This molecular pathway presents novel therapeutic targets for managing cardiac hypertrophy and related heart conditions.