Luiz Bechara

Stanford University, Chemical and Systems Biology, Post-Doc

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Papers by Luiz Bechara

Preventive effects of exercise training on dexamethasone‐induced hypertension, oxidative stress and peripheral insulin resistance

The FASEB Journal, 2010

Effect of lactate on intermediary metabolites expression and mitochondrial biogenesis in perfused hearts (864.5)

The FASEB Journal, 2014

The aim of this study was to investigate whether lactate would modulates the expression of genes ... more

Effect of FKBP12-Derived Intracellular Peptides on Rapamycin-Induced FKBP–FRB Interaction and Autophagy

Cells, 2022

Intracellular peptides (InPeps) generated by proteasomes were previously suggested as putative na... more Intracellular peptides (InPeps) generated by proteasomes were previously suggested as putative natural regulators of protein–protein interactions (PPI). Here, the main aim was to investigate the intracellular effects of intracellular peptide VFDVELL (VFD7) and related peptides on PPI. The internalization of the peptides was achieved using a C-terminus covalently bound cell-penetrating peptide (cpp; YGRKKRRQRRR). The possible inhibition of PPI was investigated using a NanoBiT® luciferase structural complementation reporter system, with a pair of plasmids vectors each encoding, simultaneously, either FK506-binding protein (FKBP) or FKBP-binding domain (FRB) of mechanistic target of rapamycin complex 1 (mTORC1). The interaction of FKBP–FRB within cells occurs under rapamycin induction. Results shown that rapamycin-induced interaction between FKBP–FRB within human embryonic kidney 293 (HEK293) cells was inhibited by VFD7-cpp (10–500 nM) and FDVELLYGRKKRRQRRR (VFD6-cpp; 1–500 nM); additi...

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and Remodeling in Heart Failure Mice

The use of b-blockers is mandatory for counteracting heart failure (HF)-induced chronic sympathet... more The use of b-blockers is mandatory for counteracting heart failure (HF)-induced chronic sympathetic hyperactivity, cardiac dysfunction and remodeling. Importantly, aerobic exercise training, an efficient nonpharmacological therapy to HF, also counteracts sympathetic hyperactivity in HF and improves exercise tolerance and cardiac contractility; the latter associated with changes in cardiac Ca2+ handling. This study was undertaken to test whether combined b–blocker and aerobic exercise training would integrate the beneficial effects of isolated therapies on cardiac structure, contractility and cardiomyocyte Ca2+ handling in a genetic model of sympathetic hyperactivity-induced HF (a2A/a2C- adrenergic receptor knockout mice,

Exercise training prevents myocardial infarction induced‐skeletal muscle atrophy by reducing oxidative stress in rats (1163.6)

The FASEB Journal, 2014

Heart failure (HF) is a syndrome that compromises not only cardiovascular system, but other tissu... more Heart failure (HF) is a syndrome that compromises not only cardiovascular system, but other tissues, such as skeletal muscle. Skeletal muscle atrophy (SMA) is an independent predictor of mortality and oxidative stress is one of factors related to this atrophy. The objective of this study was to evaluate the role of oxidative stress in SMA induced by HF and the effect of aerobic exercise training (AET) in modulating this mechanism. Male rats were randomly assigned into groups: myocardial infarction (MI) and fictitious surgery (SHAM). These groups were submitted or not to 8 weeks of AET (1h running sessions at 60%VO2max) and were named sedentary or trained (MI-SED; MI-T; SHAM-SED; SHAM-T). All the values were presented as mean ± SE. To compare results, two-way ANOVA was applied with Duncan pos hoc when necessary (p<0.05). The MI-SED rats presented reduced plantaris cross-sectional and AET prevented this atrophy and improved exercise tolerance in MI-T. MI induced oxidative stress and AET attenuated oxidative...

O exercício físico prolongado melhora a resposta vasodilatadora dependente do endotélio, porém aumenta a produção de superóxido em anéis aórticos de ratos

Exercise training reverses cancer-induced oxidative stress and decrease in muscle COPS2/TRIP15/ALIEN

Molecular Metabolism, 2020

This is a PDF file of an article that has undergone enhancements after acceptance, such as the ad... more This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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Exercise prevents impaired autophagy and proteostasis in a model of neurogenic myopathy

Scientific reports, Jan 7, 2018

Increased proteolytic activity has been widely associated with skeletal muscle atrophy. However, ... more Increased proteolytic activity has been widely associated with skeletal muscle atrophy. However, elevated proteolysis is also critical for the maintenance of cellular homeostasis by disposing cytotoxic proteins and non-functioning organelles. We recently demonstrated that exercise activates autophagy and re-establishes proteostasis in cardiac diseases. Here, we characterized the impact of exercise on skeletal muscle autophagy and proteostasis in a model of neurogenic myopathy induced by sciatic nerve constriction in rats. Neurogenic myopathy, characterized by progressive atrophy and impaired contractility, was paralleled by accumulation of autophagy-related markers and loss of acute responsiveness to both colchicine and chloroquine. These changes were correlated with elevated levels of damaged proteins, chaperones and pro-apoptotic markers compared to control animals. Sustained autophagy inhibition using chloroquine in rats (50 mg.kg.day) or muscle-specific deletion of Atg7 in mice ...

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Effects of N-acetylcysteine on isolated skeletal muscle contractile properties after an acute bout of aerobic exercise

Life sciences, Jan 15, 2017

The current study tested the hypotheses that 1) an acute bout of aerobic exercise impairs isolate... more The current study tested the hypotheses that 1) an acute bout of aerobic exercise impairs isolated skeletal muscle contractile properties and 2) N-acetylcysteine (a thiol antioxidant; NAC) administration can restore the impaired muscle contractility after exercise. At rest or immediately after an acute bout of aerobic exercise, extensor digitorum longus (EDL) and soleus muscles from male Wistar rats were harvested for ex vivo skeletal muscle contraction experiments. Muscles from exercised animals were incubated in Krebs Ringer's buffer in absence or presence of 20mM of NAC. Force capacity and fatigue properties were evaluated. Exercised EDL and soleus displayed lower force production across various stimulation frequencies (p<0.001), indicating that skeletal muscle force production was impaired after an acute bout of exercise. However, NAC treatment restored the loss of force production in both EDL and soleus after fatiguing exercise (p<0.05). Additionally, NAC treatment in...

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Aerobic Swim Training Restores Aortic Endothelial Function by Decreasing Superoxide Levels in Spontaneously Hypertensive Rats

Clinics (Sao Paulo, Brazil), 2017

We aimed to determine whether aerobic training decreases superoxide levels, increases nitric oxid... more We aimed to determine whether aerobic training decreases superoxide levels, increases nitric oxide levels, and improves endothelium-dependent vasodilation in the aortas of spontaneously hypertensive rats. Spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY) were distributed into 2 groups: sedentary (SHRsd and WKYsd, n=10 each) and swimming-trained (SHRtr, n=10 and WKYtr, n=10, respectively). The trained group participated in training sessions 5 days/week for 1 h/day with an additional work load of 4% of the animal's body weight. After a 10-week sedentary or aerobic training period, the rats were euthanized. The thoracic aortas were removed to evaluate the vasodilator response to acetylcholine (10-10 to 10-4 M) with or without preincubation with L-NG-nitro-L-arginine methyl ester hydrochloride (L-NAME; 10-4 M) in vitro. The aortic tissue was also used to assess the levels of the endothelial nitric oxide synthase and nicotinamide adenine dinucleotide oxidase subunit i...

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Mitochondrial Quality Control in Cardiac Diseases

Frontiers in physiology, 2016

Disruption of mitochondrial homeostasis is a hallmark of cardiac diseases. Therefore, maintenance... more Disruption of mitochondrial homeostasis is a hallmark of cardiac diseases. Therefore, maintenance of mitochondrial integrity through different surveillance mechanisms is critical for cardiomyocyte survival. In this review, we discuss the most recent findings on the central role of mitochondrial quality control processes including regulation of mitochondrial redox balance, aldehyde metabolism, proteostasis, dynamics, and clearance in cardiac diseases, highlighting their potential as therapeutic targets.

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Mitochondrial-derived vesicles: a new player in cardiac mitochondrial quality control

The Journal of physiology, 2016

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Exercise, Nitric Oxide, and ROS

Reactive Oxygen Species in Biology and Human Health, 2016

Efeitos do treinamento físico aeróbio sobre a bioatividade do óxido nítrico e a vasodilatação aórtica

Revista Brasileira de Educação Física e Esporte, Dec 1, 2006

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Abstract 17772: Lack of 2-adrenoceptors Accelerates Skeletal Muscle Atrophy in Myocardial Infarcted Mice: Role of Ubiquitin-Proteasome System and Akt/mTOR Pathway

Circulation, Nov 20, 2012

Although heart failure (HF) is a syndrome of cardiac origin, it promotes changes in other tissues... more

Efeitos dos treinamentos físicos aeróbico e resistido sobre a atrofia muscular esquelética na insuficiência cardíaca

A insuficiência cardíaca é uma síndrome que envolve múltiplos sistemas e mecanismos compensatório... more A insuficiência cardíaca é uma síndrome que envolve múltiplos sistemas e mecanismos compensatórios neuro-hormonais, acompanhada de altos índices de morbidade e mortalidade, caracterizada por sintomas clínicos como fadiga, dispneia e intolerância aos esforços físicos. Além do comprometimento cardíaco, observam-se importantes alterações periféricas, como a atrofia muscular esquelética, a qual contribui para o mau prognóstico e para o aumento da mortalidade dos pacientes. Estudos têm demonstrado que essa atrofia muscular pode ser causada por um desbalanço entre vias de síntese e degradação proteica, principalmente pelo aumento da ativação do sistema proteolítico ubiquitina-proteassoma e pela diminuição da ativação da via IGF-1/Akt. O treinamento físico, estratégia não farmacológica no tratamento da insuficiência cardíaca, tem se mostrado capaz de atenuar ou reverter o quadro de miopatia esquelética encontrado nessa síndrome. Portanto, foi objetivo da presente revisão discutir em maiore...

Papel dos receptores B2-adrenérgicos nas alterações musculoesqueléticas desencadeados pela insuficiência cardíaca

Editorial Card Res. Potentiating mitochondrial aldehyde dehydrogenase 2 to treat post-infarction heart failure (1)

NADPH oxidase hyperactivity induces plantaris atrophy in heart failure rats

International Journal of Cardiology, 2014

Background: Skeletal muscle wasting is associated with poor prognosis and increased mortality in ... more Background: Skeletal muscle wasting is associated with poor prognosis and increased mortality in heart failure (HF) patients. Glycolytic muscles are more susceptible to catabolic wasting than oxidative ones. This is particularly important in HF since glycolytic muscle wasting is associated with increased levels of reactive oxygen species (ROS). However, the main ROS sources involved in muscle redox imbalance in HF have not been characterized. Therefore, we hypothesized that NADPH oxidases would be hyperactivated in plantaris muscle of infarcted rats, contributing to oxidative stress and hyperactivation of the ubiquitin-proteasome system (UPS), ultimately leading to atrophy. Methods: rats were submitted to myocardial infarction (MI) or Sham surgery. Four weeks after surgery, MI and Sham groups underwent eight weeks of treatment with apocynin, a NADPH oxidase inhibitor, or placebo. NADPH oxidase activity, oxidative stress markers, NF-κB activity, p38 MAPK phosphorylation, mRNA and sarcolemmal protein levels of NADPH oxidase components, UPS activation and fiber crosssectional area were assessed in plantaris muscle. Results: Plantaris of MI rats displayed atrophy associated with increased Nox2 mRNA and sarcolemmal protein levels, NADPH oxidase activity, ROS production, lipid hydroperoxides levels, NF-κB activity, p38 MAPK phosphorylation and UPS activation. NADPH oxidase inhibition by apocynin prevented MIinduced skeletal muscle atrophy by reducing ROS production, NF-κB hyperactivation, p38 MAPK phosphorylation and proteasomal hyperactivity. Conclusion: Our data provide evidence for NADPH oxidase hyperactivation as an important source of ROS production leading to plantaris atrophy in heart failure rats, suggesting that this enzyme complex plays key role in skeletal muscle wasting in HF.

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Efeito da suplementação de creatina, associada ou não ao treinamento de força, sobre a peroxidação lipídica em mulheres idosas

Revista Brasileira de Educação Física e Esporte, 2014

O objetivo desse trabalho foi avaliar o efeito da suplementação de creatina associada ou não ao t... more O objetivo desse trabalho foi avaliar o efeito da suplementação de creatina associada ou não ao treinamento de força sobre a peroxidação lipídica em mulheres idosas. Foi conduzido um estudo clínico, randomizado, duplo-cego e controlado por placebo, no qual mulheres idosas foram randomizadas para compor quatro grupos: 1) suplementação com placebo (PL; n = 10); 2) suplementação com creatina (CR; n = 10); 3) suplementação com placebo associado ao treinamento de força (PL+TR; n = 6); e 4) suplementação com creatina associado ao treinamento de força (CR+TR; n = 8). Antes (PRE) e após 24 semanas (POS) de intervenção, foram coletadas amostras de sangue para posterior análise das concentrações plasmáticas de hidroperóxidos lipídicos por espectrofotometria. Nenhuma diferença estatística foi observada na concentração de hidroperóxidos lipídicos entre os grupos (PL: PRE = 48,7 ± 36,9; POS = 29,3 ± 18,8; delta = -13,0 ± 26,8; CR: PRE = 51,0 ± 46,0; POS = 54,2 ± 51,6; delta = -8,6 ± 30,2; PL+TR:...

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Luiz Bechara

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