Inhibition of Myocardin-related Transcription Factor A Ameliorates Pathological Remodeling of the Pressure-loaded Right Ventricle

Right ventricular (RV) fibrosis is associated with RV dysfunction in a variety of RV pressure-loading conditions in which RV mechanical stress is increased, but the underlying mechanisms driving RV fibrosis are incompletely understood. In pulmonary and cardiovascular diseases characterized by elevated mechanical stress and transforming growth factor-β1 signaling, myocardin-related transcription factor A (MRTF-A) is a mechanosensitive protein critical to driving myofibroblast transition and fibrosis. In this study, we investigated whether MRTF-A inhibition improves RV profibrotic remodeling and function in response to a pulmonary artery banding (PAB) model of RV pressure loading. Rats were assigned into either sham or PAB groups. MRTF-A inhibitor CCG-1423 was administered daily at 0.75 mg/kg in a subset of PAB animals. Echocardiography and pressure-volume hemodynamics were obtained at a terminal experiment 6 weeks later. RV myocardial samples were analyzed for fibrosis, cardiomyocyte hypertrophy, and profibrotic signaling. MRTF-A inhibition slightly reduced systolic dysfunction in PAB rats reflected by increased lateral tricuspid annulus peak systolic velocity, whereas diastolic function parameters were not significantly improved. RV remodeling was attenuated in PAB rats with MRTF-A inhibition, displaying reduced fibrosis. This was accompanied with a reduction in PAB-induced upregulation of Yes-associated protein (YAP) and its paralog transcriptional coactivator with PDZ-binding motif (TAZ). We also confirmed, using a second-generation MRTF-A inhibitor CCG-203971, that MRTF-A is critical in driving RV fibroblast expression of TAZ and markers of myofibroblast transition in response to transforming growth factor-β1 stress and RhoA activation. These studies identify RhoA, MRTF-A, and YAP/TAZ as interconnected regulators of profibrotic signaling in RV pressure loading and as potential targets to improve RV profibrotic remodeling.

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Journal
American Journal of Respiratory Cell and Molecular Biology
Published
2024-08-21
DOI
https://doi.org/10.1165/rcmb.2023-0465oc
Citations
2
Primary Topic
Cardiovascular Function and Risk Factors
Type
article
Field-Weighted Citation Impact
0.80
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article

Inhibition of Myocardin-related Transcription Factor A Ameliorates Pathological Remodeling of the Pressure-loaded Right Ventricle

Kana Yazaki, John Dauz, Golam Kabir, Wolfgang M. Kuebler et al.
2 citations
American Journal of Respiratory Cell and Molecular Biology
Cardiovascular Function and Risk Factors
0.80
article

Inhibition of Myocardin-related Transcription Factor A Ameliorates Pathological Remodeling of the Pressure-loaded Right Ventricle

Kana Yazaki, John Dauz, Golam Kabir, Wolfgang M. Kuebler, András Kapùs, Kim A. Connelly, Théo A Meister, Sonja Raschzok, Mark K. Friedberg, Xavier Lee, Linda Nghiem, Mei Sun, Jean‐François Desjardins, Mark F Rzepka
article en
2 citations

Abstract

Right ventricular (RV) fibrosis is associated with RV dysfunction in a variety of RV pressure-loading conditions in which RV mechanical stress is increased, but the underlying mechanisms driving RV fibrosis are incompletely understood. In pulmonary and cardiovascular diseases characterized by elevated mechanical stress and transforming growth factor-β1 signaling, myocardin-related transcription factor A (MRTF-A) is a mechanosensitive protein critical to driving myofibroblast transition and fibrosis. In this study, we investigated whether MRTF-A inhibition improves RV profibrotic remodeling and function in response to a pulmonary artery banding (PAB) model of RV pressure loading. Rats were assigned into either sham or PAB groups. MRTF-A inhibitor CCG-1423 was administered daily at 0.75 mg/kg in a subset of PAB animals. Echocardiography and pressure-volume hemodynamics were obtained at a terminal experiment 6 weeks later. RV myocardial samples were analyzed for fibrosis, cardiomyocyte hypertrophy, and profibrotic signaling. MRTF-A inhibition slightly reduced systolic dysfunction in PAB rats reflected by increased lateral tricuspid annulus peak systolic velocity, whereas diastolic function parameters were not significantly improved. RV remodeling was attenuated in PAB rats with MRTF-A inhibition, displaying reduced fibrosis. This was accompanied with a reduction in PAB-induced upregulation of Yes-associated protein (YAP) and its paralog transcriptional coactivator with PDZ-binding motif (TAZ). We also confirmed, using a second-generation MRTF-A inhibitor CCG-203971, that MRTF-A is critical in driving RV fibroblast expression of TAZ and markers of myofibroblast transition in response to transforming growth factor-β1 stress and RhoA activation. These studies identify RhoA, MRTF-A, and YAP/TAZ as interconnected regulators of profibrotic signaling in RV pressure loading and as potential targets to improve RV profibrotic remodeling.

American Journal of Respiratory Cell and Molecular BiologyVol. 72(2)
St. Michael's Hospital (CA), Hospital for Sick Children (CA), Canadian Heart Research Centre (CA), Charité - Universitätsmedizin Berlin (DE)
Good health and well-being
Openalex Percentile: Top 24%
Cardiovascular Function and Risk Factors
0.80
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