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• W2316392413 abstract "Purpose: Recent studies showed the involvement of Neuregulin (NRG)-1 in the preservation of left ventricular performance in pathophysiological conditions. Nevertheless, the role of NRG-1 in pulmonary arterial hypertension (PAH) and right ventricular (RV) failure is still unknown. Therefore, the goal of this study was to evaluate the effects of a NRG-1 chronic treatment on intrinsic myocardial properties, namely on the modulation of active and passive force of cardiomyocytes isolated from the RV of animals with PAH. Methods: Male Wistar rats (180-200g) randomly received monocrotaline (MCT, 60 mg/kg, sc) or vehicle. After 14 days, animals were randomly assigned to receive treatment with either NRG-1 (40 ug/kg/day, ip) or vehicle. The study resulted in 4 experimental groups: control (CTRL, n=16); CTRL+NRG (n=15); MCT (n=13); MCT+NRG (n=18). Twenty one to 24 days after MCT administration, samples were collected for functional studies. RV samples were mechanically disrupted and incubated in relaxing solution supplemented with Triton (0.2%). Single cardiomyocytes were subsequently attached with silicone adhesive between a force transducer and a piezoelectric motor and active and passive forces were measured. Only significant results (p<0.05) are given. Results: MCT-group isolated cardiomyocytes developed higher passive force when compared to CTRL-group cells at the sarcomere lengths of 2.0 (MCT vs. CTRL: 1.90±0.43 vs. 1.43±0.29N/m2), 2.2 (MCT vs. CTRL: 3.66±0.69 vs. 2.68±0.24N/m2), and 2.3μm (MCT vs. CTRL: 5.76±1.15 vs. 3.86±0.87N/m2). NRG-1 treatment restored passive force development to levels similar to the CTRL-group cardiomyocytes, at 2.0, 2.2, and 2.3μm (MCT+NRG: 1.28±0.25, 3.04±0.55, and 3.63±0.89N/m2, respectively). CTRL+NRG-group cardiomyocytes developed significantly less passive force when compared to CTRL-group cells (CTRL+NRG: 1.16±0.31, 2.27±0.38, and 3.05±0.54N/m2, at 2.0, 2.2, and 2.3μm respectively). In the MCT+NRG-group cardiomyocytes active force development was decreased when compared to MCT-group cells (MCT vs MCT+NRG: 14.14±5.94 vs 9.67±2.83N/m2). Conclusions: NRG-1 chronic treatment reverses the changes in both active and passive myocardial forces that occur in the presence of PAH. Interestingly, NRG-1 chronic treatment also decreases the passive force and thus myocardial stiffness of cardiomyocytes isolated from the right ventricle of healthy animals. These findings show that NRG-1 pathway regulates systolic and diastolic function at the cellular level, and suggest a potential therapeutic role of this pathway in PAH." @default.
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• W2316392413 date "2013-08-02" @default.
• W2316392413 modified "2023-10-17" @default.
• W2316392413 title "Neuregulin-1 modulates right ventricle cardiomyocyte function in pulmonary arterial hypertension" @default.
• W2316392413 doi "https://doi.org/10.1093/eurheartj/eht310.p5029" @default.
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