Moderate exercise training provides left ventricular tolerance to acute pressure overload

Moreira-Gonçalves, Daniel; Henriques‐Coelho, Tiago; Fonseca, Hélder; Ferreira, Rita; Amado, Francisco; Leite‐Moreira, Adelino F.; Duarte, José Alberto

doi:10.1152/ajpheart.01008.2010

Cited by 12 publications

(8 citation statements)

References 48 publications

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“…Three assays were performed. This method is in accordance to Moreira-Gonçalves and collaborators with some modifications [25]. Three-dimensional surface plot analyses were generated with the “Surface Plot” function of Image J 1.44 (http://rsbweb.nih.gov/ij/download.html).…”

Section: Methodsmentioning

confidence: 99%

Is Nitric Oxide Decrease Observed with Naphthoquinones in LPS Stimulated RAW 264.7 Macrophages a Beneficial Property?

et al. 2011

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The search of new anti-inflammatory drugs has been a current preoccupation, due to the need of effective drugs, with less adverse reactions than those used nowadays. Several naphthoquinones (plumbagin, naphthazarin, juglone, menadione, diosquinone and 1,4-naphthoquinone), plus p-hydroquinone and p-benzoquinone were evaluated for their ability to cause a reduction of nitric oxide (NO) production, when RAW 264.7 macrophages were stimulated with lipopolysaccharide (LPS). Dexamethasone was used as positive control. Among the tested compounds, diosquinone was the only one that caused a NO reduction with statistical importance and without cytotoxicity: an IC25 of 1.09±0.24 µM was found, with 38.25±6.50% (p<0.001) NO reduction at 1.5 µM. In order to elucidate if this NO decrease resulted from the interference of diosquinone with cellular defence mechanisms against LPS or to its conversion into peroxynitrite, by reaction with superoxide radical formed by naphthoquinones redox cycling, 3-nitrotyrosine and superoxide determination was also performed. None of these parameters showed significant changes relative to control. Furthermore, diosquinone caused a decrease in the pro-inflammatory cytokines: tumour necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6). Therefore, according to the results obtained, diosquinone, studied for its anti-inflammatory potential for the first time herein, has beneficial effects in inflammation control. This study enlightens the mechanisms of action of naphthoquinones in inflammatory models, by checking for the first time the contribution of oxidative stress generated by naphthoquinones to NO reduction.

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Section: Methodsmentioning

confidence: 99%

Is Nitric Oxide Decrease Observed with Naphthoquinones in LPS Stimulated RAW 264.7 Macrophages a Beneficial Property?

et al. 2011

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“…Swim training is known to promote favorable cardiac outcomes including protection from various cardiac insults 17, 22, 23 . We have shown that when GRK5 is elevated in cardiac myocytes an early and progressive HF phenotype arises after TAC 4-6 .…”

Section: Resultsmentioning

confidence: 99%

“…Several previous studies in the literature have been performed in non-transgenic rodents to demonstrate the beneficial effects of exercise either prior to or after cardiac insult 22, 31-33 . Thus, we didn't study non-transgenic animals alone for swimming since our goal was to specifically address whether exercise in the face of cardiac-specific overexpression of GRK5 led to pathological changes and if swimming caused the nuclear localization of GRK5.…”

Section: Discussionmentioning

confidence: 99%

Differential Role of G Protein–Coupled Receptor Kinase 5 in Physiological Versus Pathological Cardiac Hypertrophy

Traynham

Cannavò

Zhou

et al. 2015

Circulation Research

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Rationale G protein-coupled receptor (GPCR) kinases (GRKs) are dynamic regulators of cellular signaling. GRK5 is highly expressed within myocardium and is up-regulated in heart failure (HF). Although GRK5 is a critical regulator of cardiac GPCR signaling, recent data has uncovered non-canonical activity of GRK5 within nuclei that plays a key role in pathological hypertrophy. Targeted cardiac elevation of GRK5 in mice leads to exaggerated hypertrophy and early HF after transverse aortic constriction (TAC) due to GRK5 nuclear accumulation. Objective In this study we investigated the role of GRK5 in physiological, swimming induced hypertrophy (SIH). Methods and Results Cardiac-specific GRK5 transgenic mice (TgGRK5) and non-transgenic littermate control (NLC) mice were subjected to a 21-day high intensity swim protocol (or no swim sham controls). SIH and specific molecular and genetic indices of physiological hypertrophy were assessed including nuclear localization of GRK5 and compared to TAC. Unlike after TAC, swim-trained TgGRK5 and NLC mice exhibited similar increases in cardiac growth. Mechanistically, SIH did not lead to GRK5 nuclear accumulation, which was confirmed in vitro as insulin-like growth factor-1, a known mediator of physiological hypertrophy, was unable to induce GRK5 nuclear translocation in myocytes. We found specific patterns of altered gene expression between TAC and SIH with GRK5 overexpression. Further, SIH in post-TAC TgGRK5 mice was able to preserve cardiac function. Conclusions These data suggest that while nuclear-localized GRK5 is a pathological mediator after stress, this non-canonical nuclear activity of GRK5 is not induced during physiological hypertrophy.

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“…The slides were dewaxed in xylene and hydrated through graded alcohols finishing in PBS solution. Deparaffinized sections of lung tissue were stained for immunohistochemical staining of rabbit anti‐HMGB1 (1:400 dilution; Abcam, Cat# ab79823, RRID:AB_1603373), using the secondary anti‐body goat biotinylated anti‐rabbit (1:200 dilution; Vector Laboratories, Cat# BA‐1000, RRID:AB_2313606) and counterstained with hematoxylin‐eosin, as previously described (Moreira‐Goncalves et al, ).…”

Section: Methodsmentioning

confidence: 99%

HMGB1 down‐regulation mediates terameprocol vascular anti‐proliferative effect in experimental pulmonary hypertension

Nogueira-Ferreira

Ferreira‐Pinto

Silva

et al. 2017

Journal Cellular Physiology

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Pulmonary arterial hypertension (PAH) is a progressive disease with a poor prognosis. Pulmonary artery smooth muscle cells (PASMCs) play a crucial role in PAH pathophysiology, displaying a hyperproliferative, and apoptotic-resistant phenotype. In the present study, we evaluated the potential therapeutic role of terameprocol (TMP), an inhibitor of cellular proliferation and promoter of apoptosis, in a well-established pre-clinical model of PAH induced by monocrotaline (MCT) and studied the biological pathways modulated by TMP in PASMCs. Wistar rats injected with MCT or saline (SHAM group) were treated with TMP or vehicle. On day 21 after injection, we assessed bi-ventricular hemodynamics and cardiac and pulmonary morphometry. The effects of TMP on PASMCs were studied in a primary culture isolated from SHAM and MCT-treated rats, using an iTRAQ-based proteomic approach to investigate the molecular pathways modulated by this drug. In vivo, TMP significantly reduced pulmonary and cardiac remodeling and improved cardiac function in PAH. In vitro, TMP inhibited proliferation and induced apoptosis of PASMCs. A total of 65 proteins were differentially expressed in PASMCs from MCT rats treated with TMP, some of which involved in the modulation of transforming growth factor beta pathway and DNA transcription. Anti-proliferative effect of TMP seems to be explained, at least in part, by the down-regulation of the transcription factor HMGB1. Our findings support the beneficial role of TMP in PAH and suggest that it may be an effective therapeutic option to be considered in the clinical management of PAH.

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Moderate exercise training provides left ventricular tolerance to acute pressure overload

Cited by 12 publications

References 48 publications

Is Nitric Oxide Decrease Observed with Naphthoquinones in LPS Stimulated RAW 264.7 Macrophages a Beneficial Property?

Is Nitric Oxide Decrease Observed with Naphthoquinones in LPS Stimulated RAW 264.7 Macrophages a Beneficial Property?

Differential Role of G Protein–Coupled Receptor Kinase 5 in Physiological Versus Pathological Cardiac Hypertrophy

HMGB1 down‐regulation mediates terameprocol vascular anti‐proliferative effect in experimental pulmonary hypertension

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