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Updated: Mar 24, 2026
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Sarcomere Shortening of Pluripotent Stem Cell-Derived Cardiomyocytes using Fluorescent-Tagged Sarcomere Proteins.
Published on: March 3, 2021
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Profilin modulates sarcomeric organization and mediates cardiomyocyte hypertrophy
Viola Kooij1, Meera C Viswanathan2, Dong I Lee2
1Department of Medicine, Division of Cardiology, The Johns Hopkins University, Baltimore, MD, USA National Heart and Lung Institute, Imperial College London, 4th floor, ICTEM, Hammersmith Campus, Du Cane Road, London W12 0NN, UK v.kooij@imperial.ac.uk.
Cardiovascular Research
|March 10, 2016
Summary
Profilin-1 is a key mediator of cardiac hypertrophy, driving increased cell size and sarcomere remodelling. Reducing profilin-1 levels can attenuate this hypertrophic response in cardiomyocytes.
Area of Science:
- Cardiovascular Biology
- Cellular Biology
- Molecular Medicine
Background:
- Cardiac hypertrophy precedes heart failure, involving increased cell size and cytoskeletal changes.
- Profilin, an actin-binding protein, has an unknown role in cardiomyocytes despite its involvement in vascular hypertrophy.
Purpose of the Study:
- To investigate the hypothesis that profilin-1 is a key mediator of cardiomyocyte-specific hypertrophic remodeling.
- To elucidate the role of profilin-1 in the development of cardiac hypertrophy.
Main Methods:
- Elevated profilin-1 levels in mouse models of hypertrophy.
- Studied profilin-1 effects in Drosophila and neonatal rat ventricular myocytes (NRVMs) via overexpression and silencing.
- Investigated the ERK1/2 signaling pathway and sarcomeric localization using confocal microscopy.
Main Results:
- Profilin-1 overexpression in NRVMs induced hypertrophy, increasing myocyte size and gene expression.
- Profilin-1 silencing attenuated phenylephrine- or endothelin-1-stimulated hypertrophic responses.
- Profilin-1 regulates hypertrophy partly via ERK1/2 signaling and causes sarcomeric disorganization and impaired muscle function.
Conclusions:
- Profilin-1 is identified as a significant mediator of cardiomyocyte hypertrophy.
- Profilin-1 overexpression is sufficient to induce cardiomyocyte hypertrophy and sarcomeric remodeling.
- Profilin-1 silencing effectively attenuates the hypertrophic response in cardiomyocytes.
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