Lipopolysaccharide exposure modulates the contractile and migratory phenotypes of vascular smooth muscle cells.

INTRODUCTION: Sepsis survivors are at higher risk for cardiovascular events. Lipopolysaccharide (LPS) activates Toll-like receptor 4 (TLR4) in sepsis. Activation of TLR4 modulates vascular smooth muscle cells (VSMCs) phenotype and contributes to cardiovascular changes after sepsis. AIM: Investigate changes in VSMCs phenotype caused by LPS-induced TLR4 activation. METHODS: Rat VSMCs were incubated with LPS. Two incubation conditions were used in cell contraction and migration assays: acute stimulation - LPS stimulus was initiated at the beginning of the assay and maintained throughout; and preconditioning - LPS stimulation was applied prior to the assay then discontinued. Nitric oxide (NO) production, mRNA expression of cytokines and phenotype markers, and interleukin (IL)-6 production were evaluated. KEY FINDINGS: LPS increased gene expression of IL-1ß, IL-6, TNFα and MCP-1 (p < .001), of secretory phenotype markers collagen and vimentin (p < .0479) and of the contractile marker smooth muscle 22α (SM22α) (p = .0067). LPS exposure increased IL-6 secretion after 24 and 48 h (p < .0001), and NO at 8 and 24 h (p < .0249) via inducible nitric oxide synthase (iNOS), as demonstrated by a decrease in NO after incubation with aminoguanidine. Acute stimulation with LPS reduced migration and contraction in a NO-dependent manner, while preconditioning with LPS increased both in an IL-6-dependent manner. SIGNIFICANCE: LPS affects VSMCs by modulating their secretory, contractile and migratory phenotypes. LPS acute stimulation of VSMCs promoted a NO-dependent reduction in migration and contraction, while preconditioning with LPS promoted IL-6-dependent increases in migration and contraction, evidencing that VSMCs can present phenotype modifications that persist after sepsis, thereby contributing to postsepsis cardiovascular events.

Blockade of AT1 receptor restore the migration of vascular smooth muscle cells in high sodium medium.

The present study aimed to test the hypothesis that increased sodium concentration affects the migratory phenotype of vascular smooth muscle cells (VSMCs) independently of the haemodynamic factors. Cell migration was evaluated by wound-healing assay under the following conditions: high sodium (HS, 160 mM) and control (CT, 140 mM). Cell viability was assessed by annexin V and propidium iodide labeling. Cyclooxygenase-2 (COX-2) gene expression was analysed by reverse transcription polymerase chain reaction. ERK1/2 phosphorylation was assessed by western blot. Exposure of VSMCs to HS reduced migration, and AT1R blockade prevented this response. HS increased COX-2 gene expression, and COX-2 blockade prevented the reduction in VSMC migration induced by HS. HS also increased ERK1/2 phosphorylation, and ERK1/2 inhibition recovered VSMC migration as well as blocked COX-2 gene expression. The TXA2 receptor blocker, but not the prostacyclin receptor blocker, prevented the HS-induced VSMCs migration decrease. HS reduces the migration of VSMCs by increasing COX-2 gene expression via AT1R-ERK1/2 phosphorylation. In addition, increased COX-2 by HS seems to modulate the reduction of VSMCs migration by the TXA2 receptor.

Effects of direct high sodium exposure at endothelial cell migration.

The present study aimed to test the hypothesis that high sodium affects the migratory phenotype of endothelial cells (EC) and investigates mechanisms involved independently of hemodynamic factors. Cell migration was evaluated by Wound-Healing at conditions: High Sodium (HS; 160 mM) and Control (CT; 140 mM). O2- production was evaluated by DHE. NADPH oxidase activity was determined by chemiluminescence assay. Expression of adhesion molecules was analyzed by RT-PCR. Shear Stress was performed using a rhythmic shake. Nitric oxide production was measured by Griess reaction. HS-induced impairment in EC migration while both Candesartan and DPI prevented it. HS increased NADPH oxidase activity, which was blocked by Candesartan. Also, HS increased O2- production that was inhibited by Candesartan. HS decreased adhesion molecules expression via ROS (Integrin Alpha 5, Integrin Beta 1, Integrin Beta 3, VE-Cadherin and PECAM) and via AT1R (PECAM). The nitric oxide production induced by shear stress was decreased after EC exposure to HS while both Candesartan and DPI prevented it. Conclusion: This study demonstrated that HS reduced EC migration by AT1R and ROS derived from NADPH Oxidase and mitochondria. The HS reduction in adhesion molecules expression modulated by ROS and AT1R may help to explain the impairment in migration capacity. Also, HS affected EC functionality by reducing their nitric oxide production in response to shear stress.

Dipeptidyl peptidase-4 inhibition prevents vascular dysfunction induced by ß-adrenergic hyperactivity.

Chronic stimulation of the ß-adrenergic sympathetic system induces vascular dysfunction which is associated with increased inflammatory cytokines production. A recently proposed therapy to control vascular injury through inflammatory processes involves inhibition of the enzyme dipeptidyl peptidase-IV (DPP4). The present study investigates whether the inhibition of DPP4 prevents the increase in inflammatory markers induced by isoproterenol and restores endothelial function in vivo and in vitro. Male Wistar rats were divided into four groups: vehicle (VHC), an isoproterenol-treated group (ISO), a sitagliptin-treated group (SITA), and an isoproterenol and sitagliptin-treated group (ISO + SITA). The ISO group exhibited significantly increased contractile responses to phenylephrine associated with reduced endothelial participation, which was totally prevented by DPP4 inhibition. In vitro incubation with isoproterenol had no effect on vascular smooth muscle cells, however isoproterenol increased the activity of DPP4 and the expression of inflammatory cytokines in endothelial cells, while sitagliptin reduced the level of cytokines to basal level. In conclusion, we have shown that beta-adrenergic receptor activation can increase DPP4 activity, which was associated with vascular dysfunction and cytokine expression in endothelial cells. The important role of DPP4 was further supported by sitagliptin, which reversed vascular changes induced by isoproterenol in vivo and in vitro.

Exercise Training and Epigenetic Regulation: Multilevel Modification and Regulation of Gene Expression.

Exercise training elicits acute and adaptive long term changes in human physiology that mediate the improvement of performance and health state. The responses are integrative and orchestrated by several mechanisms, as gene expression. Gene expression is essential to construct the adaptation of the biological system to exercise training, since there are molecular processes mediating oxidative and non-oxidative metabolism, angiogenesis, cardiac and skeletal myofiber hypertrophy, and other processes that leads to a greater physiological status. Epigenetic is the field that studies about gene expression changes heritable by meiosis and mitosis, by changes in chromatin and DNA conformation, but not in DNA sequence, that studies the regulation on gene expression that is independent of genotype. The field approaches mechanisms of DNA and chromatin conformational changes that inhibit or increase gene expression and determine tissue specific pattern. The three major studied epigenetic mechanisms are DNA methylation, Histone modification, and regulation of noncoding RNA-associated genes. This review elucidates these mechanisms, focusing on the relationship between them and their relationship with exercise training, physical performance and the enhancement of health status. On this chapter, we clarified the relationship of epigenetic modulations and their intimal relationship with acute and chronic effect of exercise training, concentrating our effort on skeletal muscle, heart and vascular responses, that are the most responsive systems against to exercise training and play crucial role on physical performance and improvement of health state.

Exercise training restores the cardiac microRNA-1 and -214 levels regulating Ca2+ handling after myocardial infarction.

BACKGROUND: Impaired cardiomyocyte contractility and calcium handling are hallmarks of left ventricular contractile dysfunction. Exercise training has been used as a remarkable strategy in the treatment of heart disease. The microRNA-1, which targets sodium/calcium exchanger 1 (NCX), and microRNA-214, which targets sarcoplasmic reticulum calcium ATPase-2a (Serca2a), are involved in cardiac function regulation. Thus, the aim of this study was to evaluate the effect of exercise training on cardiac microRNA-1 and -214 expression after myocardial infarction. METHODS: Wistar rats were randomized into four groups: sedentary sham (S-SHAM), sedentary infarction (S-INF), trained sham (T-SHAM), and trained infarction (T-INF). Exercise training consisted of 60 min/days, 5 days/week for 10 weeks with 3 % of body weight as overload beginning four weeks after myocardial infarction. RESULTS: MicroRNA-1 and -214 expressions were, respectively, decreased (52 %) and increased (54 %) in the S-INF compared to the S-SHAM, while exercise training normalized the expression of these microRNAs. The microRNA targets NCX and Serca-2a protein expression were, respectively, decreased (55 %) and increased (34 %) in the T-INF group compared to the S-INF group. CONCLUSIONS: These results suggest that exercise training restores microRNA-1 and -214 expression levels and prevents change in both NCX and Serca-2a protein and gene expressions. Altogether, our data suggest a molecular mechanism to restore ventricular function after exercise training in myocardial infarction rats.

Resistance training regulates cardiac function through modulation of miRNA-214.

AIMS: To determine the effects of resistance training (RT) on the expression of microRNA (miRNA)-214 and its target in sarcoplasmic reticulum Ca2+-ATPase (SERCA2a), and on the morphological and mechanical properties of isolated left ventricular myocytes. MAIN METHODS: Male Wistar rats were divided into two groups (n = 7/group): Control (CO) or trained (TR). The exercise-training protocol consisted of: 4 × 12 bouts, 5×/week during 8 weeks, with 80% of one repetition maximum. KEY FINDINGS: RT increased the left ventricular myocyte width by 15% and volume by 12%, compared with control animals (p < 0.05). The time to half relaxation and time to peak were 8.4% and 4.4% lower, respectively, in cells from TR group as compared to CO group (p < 0.05). RT decreased miRNA-214 level by 18.5% while its target SERCA2a expression were 18.5% higher (p < 0.05). SIGNIFICANCE: Our findings showed that RT increases single left ventricular myocyte dimensions and also leads to faster cell contraction and relaxation. These mechanical adaptations may be related to the augmented expression of SERCA2a which, in turn, may be associated with the epigenetic modification of decreased miRNA-214 expression.

Exercise training in hypertension: Role of microRNAs.

Hypertension is a complex disease that constitutes an important public health problem and demands many studies in order to understand the molecular mechanisms involving his pathophysiology. Therefore, an increasing number of studies have been conducted and new therapies are continually being discovered. In this context, exercise training has emerged as an important non-pharmacological therapy to treat hypertensive patients, minimizing the side effects of pharmacological therapies and frequently contributing to allow pharmacotherapy to be suspended. Several mechanisms have been associated with the pathogenesis of hypertension, such as hyperactivity of the sympathetic nervous system and renin-angiotensin aldosterone system, impaired endothelial nitric oxide production, increased oxygen-reactive species, vascular thickening and stiffening, cardiac hypertrophy, impaired angiogenesis, and sometimes genetic predisposition. With the advent of microRNAs (miRNAs), new insights have been added to the perspectives for the treatment of this disease, and exercise training has been shown to be able to modulate the miRNAs associated with it. Elucidation of the relationship between exercise training and miRNAs in the pathogenesis of hypertension is fundamental in order to understand how exercise modulates the cardiovascular system at genetic level. This can be promising even for the development of new drugs. This article is a review of how exercise training acts on hypertension by means of specific miRNAs in the heart, vascular system, and skeletal muscle.

Expression of MicroRNA-29 and Collagen in Cardiac Muscle after Swimming Training in Myocardial-Infarcted Rats.

BACKGROUND: Myocardial infarction (MI) is accompanied by cardiac growth, increased collagen deposition, cell death and new vascularization of the cardiac tissue, which results in reduced ventricular compliance. The MiRNA-29 family (29a, 29b, and 29c) targets mRNAs that encode collagens and other proteins involved in fibrosis. In this study we assessed the effects of swimming training (ST) on expression of the cardiac miRNA-29 family and on genes encoding collagen after MI in rats. METHODS: ST consisted of 60 min/day/10 weeks and began four weeks after MI. MiRNA and collagen expression analysis were performed in the infarcted region (IR), border region (BR) of the infarcted region and in the remote myocardium (RM) of the left ventricle. RESULTS: MiRNA-29a expression increased 32% in BR and 52% in RM in the TR-INF compared with SED-INF. MiRNA-29c increased by 63% in BR and 55% in RM in TR-INF compared with SED-INF group. COL IAI and COL IIIAI decreased by 63% and 62% in TR-INF, respectively, compared with SED-INF. COLIIIAI expression decreased by 16% in TR-INF compared with SED-INF. CONCLUSION: Altogether, our results showed that ST restores cardiac miRNA-29 (a and c) levels and prevents COL IAI and COL IIIAI expression in BR and RM, which may contribute to the improvement in ventricular function induced by swimming training, after MI. © 2014 S. Karger AG, Basel.

Exercício de força ativa a via AKT/mTor pelo receptor de angiotensina II tipo I no músculo cardíaco de ratos / Activation of AKT-mTor signaling pathways by angiotensin II receptor type 1 after a session of strength exercise in cardiac muscle of rats

O receptor de angiotensina II tipo I (AT1) tem uma importante participação no desenvolvimento da hipertrofia cardíaca. Em um trabalho publicado anteriormente, por nosso grupo, demonstramos que o bloqueio do receptor AT1 durante o treinamento de força inibiu a hipertrofia cardíaca em ratos. Por isso, o objetivo deste trabalho foi estudar a participação do receptor AT1 na ativação de vias de sinalização intracelular relacionadas com o aumento da síntese de proteína em ratos submetidos a uma sessão de exercício de força. Para isso, realizamos um experimento com seis grupos de animais (n = 6; cada): controle (Con), exercitado e sacrificado cinco minutos após o exercício (Exe 5), exercitado e sacrificado 30 minutos após o exercício (Exe 30), controle tratado com losartan (Con Los), tratado com losartan, exercitado e sacrificado cinco minutos após o exercício (Exe 5 Los), tratado com losartan, exercitado e sacrificado 30 minutos após o exercício (Exe 30 Los). Os resultados mostram que no grupo Exe 5 e Exe 30 ocorreu um aumento de 63 por cento (P < 0,05) e 62 por cento (P < 0,05), respectivamente, na fosforilação da proteína AKT comparado com o grupo controle. Enquanto a fosforilação da mTor foi aumentada 65 por cento (P < 0,05) somente no grupo Exe 30 comparado com o grupo controle, sendo estes efeitos bloqueados pelo uso do losartan nos grupos Exe 5 Los e Exe 30 Los. Portanto, esses resultados, juntamente com nossos resultados prévios, demonstram que o receptor AT1 tem participação na ativação da AKT e mTOR após uma sessão de exercício de força.

The angiotensin II type I (AT1) receptor has an important participation in the development of cardiac hypertrophy. Previously, we have shown that AT1 receptor participates in the cardiac hypertrophy induced by resistance training in rats. Here, we studied the involvement of AT1 receptor in the activation of intracellular signaling pathways related to the concentric HC in rats submitted to a session of strength exercise. Male Wistar rats were divided into 6 groups (n= 6 each): control (Con); exercised and killed 5 minutes after exercise (Exe 5); exercised and killed 30 minutes after exercise (Exe 30); control treated with Losartan (Con Los); treated with Losartan, exercised and killed 5 minutes after the exercise (Exe Los 5); treated with Losartan, exercised and killed 30 minutes after training (Exe Los 30). The results show that phosphorylation activity of AKT in group Exe 5 and Exe 30 increased 63 percent (P < 0.05) and 62 percent (P < 0.05), respectively, compared with Con. Whereas the phosphorylation of mTOR was increased 65 percent (P < 0.05), compared to Con, only in the group Exe 30. Furthermore, these effects were blocked by losartan treatment in groups Exe Los 5 and Exe Los 30. These results, together with ours previous data shows that the AT1 receptor has an role in the activation of AKT and mTOR pathway after a session of strength exercise.

Anabolic steroid associated to physical training induces deleterious cardiac effects.

PURPOSE: Cardiac aldosterone might be involved in the deleterious effects of nandrolone decanoate (ND) on the heart. Therefore, we investigated the involvement of cardiac aldosterone, by the pharmacological block of AT1 or mineralocorticoid receptors, on cardiac hypertrophy and fibrosis. METHODS: Male Wistar rats were randomized into eight groups (n = 14 per group): Control (C), nandrolone decanoate (ND), trained (T), trained ND (TND), ND + losartan (ND + L), trained ND + losartan (TND + L), ND + spironolactone (ND + S), and trained ND + spironolactone (TND + S). ND (10 mg·kg(-1)·wk(-1)) was administered during 10 wk of swimming training (five times per week). Losartan (20 mg·kg(-1)·d(-1)) and spironolactone (10 mg·kg(-1)·d(-1)) were administered in drinking water. RESULTS: Cardiac hypertrophy was increased 10% by using ND and 17% by ND plus training (P < 0.05). In both groups, there was an increase in the collagen volumetric fraction (CVF) and cardiac collagen type III expression (P < 0.05). The ND treatment increased left ventricle-angiotensin-converting enzyme I activity, AT1 receptor expression, aldosterone synthase (CYP11B2), and 11-ß hydroxysteroid dehydrogenase 2 (11ß-HSD2) gene expression and inflammatory markers, TGFß and osteopontin. Both losartan and spironolactone inhibited the increase of CVF and collagen type III. In addition, both treatments inhibited the increase in left ventricle-angiotensin-converting enzyme I activity, CYP11B2, 11ß-HSD2, TGFß, and osteopontin induced by the ND treatment. CONCLUSIONS: We believe this is the first study to show the effects of ND on cardiac aldosterone. Our results suggest that these effects may be associated to TGFß and osteopontin. Thus, we conclude that the cardiac aldosterone has an important role on the deleterious effects on the heart induced by ND.

Efeitos do treinamento em natação abaixo do limiar de lactato sobre a expressão de proteínas de estresse (Hsp72) no miocárdio de ratos / Effects of swimming training below lactate threshold on the expression of stress proteins (hsp72) in the myocardium of rats

Os objetivos deste estudo foram testar se programas de natação com intensidades abaixo do limiar de lactato induzem a expressão de proteínas de estresse (Hsp72) no miocárdio de ratos e se a indução da expressão de Hsp72 é distinta nos ventrículos direito e esquerdo. Ratos Wistar foram alocados randomicamente em três grupos: controle (C, n = 8); natação sem sobrecarga (NSS, n = 8); e natação com sobrecarga - 3% do peso corporal (NCS, n = 8). Animais NSS e NCS nadaram 30 minutos/dia, cinco dias/semana, durante sete semanas. Após eutanásia, o coração foi removido, pesado e foram coletados fragmentos dos ventrículos direito (VD) e esquerdo (VE) para análise dos níveis de Hsp72. O peso relativo do coração não foi diferente (p=0,68) entre os grupos (C=4,52 ± 0,87; NSS= 4,54 ± 0,79; NCS=4,72 ± 0,16 mg/g). Os níveis de Hsp72 foram maiores no VE do grupo NCS do que no C (396,29 ± 11,91 vs. 321,04 ± 9,65 unidade arbitrária, respectivamente; p = 0,0006). Hsp72 no VE do grupo NCS foram maiores que no NSS (396,29 ± 11,91 vs. 339,43 ± 10,21 unidade arbitrária, respectivamente; p = 0,004). Não houve diferença de Hsp72 no VD entre os grupos (C=320,02 ± 10,35; NSS=321,53 ± 24,8; NCS=353,08 ± 23,44 unidade arbitrária; p = 0,47). Não houve diferença na expressão de Hsp72 entre VD e VE nos grupos (C, p=0,94; NSS, p=0,52; NCS, p=0,11). Concluiu-se que o programa de natação com intensidade abaixo do limiar de lactato (3% do peso corporal) induz a expressão de HSP 72 no miocárdio de ratos, especialmente no ventrículo esquerdo.

We tested whether swimming training regimes of different intensities bellow the anaerobic threshold induce expression of stress protein (Hsp72) in rat’s myocardium; and if the expression of Hsp72 differs between left and right ventricles. Wistar rats (6 weeks of age, body weight of ~ 261 g) were allocated into three groups: control (C, n = 8); unloaded swimming (NSS, n = 8); and loaded swimming - 3% body weight (NCS, n = 8). Animals from NSS and NCS swam 30 min/day, 5 days/week, during 7 days. At sacrifice the heart was removed and weighed. Fragments of right (RV) and left ventricles (LV) were harvested and the levels of Hsp72 determined. The heart weight to body weight ratio did not differ among C, NSS and NCS groups (4.52 ± 0.87; 4.54 ± 0.79; 4.72 ± 0.16 mg/g, respectively). The LV levels of Hsp72 were higher in NCS group than in C (396.29 ± 11.91 vs. 321.04 ± 9.65 arbitrary unit, respectively, p = 0.0006). The LV levels of Hsp72 were higher in NCS than in NSS (396.29 ± 11.91 vs. 339.43 ± 10.21 arbitrary unit, respectively; p = 0.004). There was no difference in RV levels of Hsp72 among groups (C=320.02 ± 10.35; NSS=321.53 ± 24.80; NCS=353.08 ± 23.44 arbitrary unit; p = 0.47). There was no difference in Hsp72 levels between RV and LV among groups (C, p=0.94; NSS, P=0.52; NCS, p=0.11). It was concluded that the swimming training program with intensity bellow the anaerobic threshold (3% body weight) induces expression of Hsp72 in the rat myocardium, especially in the left ventricle.

Níveis distintos de Hsp72 no miocárdio de ratas em resposta aos exercícios voluntário e forçado / Different levels of Hsp72 in female rat myocardium in response to voluntary exercise and forced exercise / Niveles distintos de Hsp72 en el miocardio de ratas en respuesta a los ejercicios voluntario y forzado

FUNDAMENTO: O exercício físico promove estresse hemodinâmico. OBJETIVO: Testar se programas de treinamento com corridas voluntária e forçada induzem níveis distintos de expressão de Hsp72 no miocárdio de ratas Wistar. MÉTODOS: Ratas Wistar foram alocadas em três grupos (n = 6, cada): treinadas com corrida voluntária (TCV), treinadas com corrida forçada (TCF) e grupo controle (C). Os animais do TCV tiveram livre acesso à roda de corrida voluntária, enquanto os do TCF foram submetidos à corrida forçada em esteira (18 m/min, 0 por cento inclinação, 60 m/min, 5 dias/sem) durante oito semanas. Fragmentos dos ventrículos esquerdo (VE) e direito (VD) foram coletados para análise dos níveis de Hsp72. RESULTADOS: As ratas do grupo TCV correram, em média, 4,87 km, e as do TCF, 4,88 km por semana. Os animais dos grupos TCV e TCF ganharam menos peso (p < 0,05) que os do grupo C (81,67 ± 11,95 g vs 81,17 ± 10,18 g vs 111,50 ± 2,26 g, respectivamente). O peso relativo do coração não foi diferente (p > 0,05) entre os grupos TCV, TCF e C (4,54 ± 0,79 mg/g vs 4,94 ± 0,89 mg/g vs 4,34 ± 0,87 mg/g, respectivamente). Ratas treinadas com corrida forçada apresentaram níveis de Hsp72 maiores (p < 0,05) que as que correram voluntariamente, no VE (287,45 ± 35,86 por cento vs 135,59 ± 5,10 por cento, respectivamente) e no VD (241,31 ± 25,83 por cento vs 137,91 ± 45,20 por cento, respectivamente). CONCLUSÃO: Os programas de treinamento com corrida voluntária e forçada induziram níveis distintos de expressão de Hsp72 no miocárdio de ratas Wistar.

BACKGROUND: Physical exercise induces hemodynamic stress. OBJECTIVE: To evaluate if voluntary running and forced running induced different levels of stress protein (Hsp72) in the myocardium of female Wistar rats. METHODS: Female rats were randomly assigned to the following groups: forced treadmill running group (FR; n= 6), voluntary running group (VR; n=6) and control group (C; n=6). VR group animals had free access to running wheels, and those from FR group underwent a running program on a treadmill (18 m/min, 60 min/day, 5 days/wk) for 8 weeks. Left ventricle (LV) and right ventricle (RV) fragments were collected at sacrifice, and the relative immunoblot contents of stress protein (Hsp72) were determined. RESULTS: VR animals ran on average 4.87 km/wk, and FR rats ran 4.88 km/wk. Animals from VR and FR groups had less body weight gain (p<0.05) than those from C group (81.67 ± 11.95g vs 81.17 ± 10.18g vs 111.50 ± 2.26g, respectively). Heart weight/body weight ratio was not significantly different (p>0.05) among VR, FR and C groups (4.54 ± 0.79 mg/g vs 4.94 ± 0.89 mg/g vs 4.34 ± 0.87 mg/g, respectively). FR group animals had levels of Hsp72 (p<0.05) higher than those from VR, both in LV (287.45 ± 35.86 percent vs 135.59 ± 5.10 percent, respectively) and RV (241.31 ± 25.83 percent vs 137.91 ± 45.20 percent, respectively). CONCLUSION: Voluntary running and forced running induced different levels of Hsp72 in the myocardium of female Wistar rats.

FUNDAMENTO: El ejercicio físico promueve estrés hemodinámico. OBJETIVO: Probar si programas de entrenamiento con carreras voluntaria y forzada inducen niveles distintos de expresión de Hsp72 en el miocardio de ratas hembra Wistar. MÉTODOS: Ratas hembra Wistar fueron distribuidas en tres grupos (n = 6, cada uno): entrenadas con carrera voluntaria (ECV), entrenadas con carrera forzada (ECF) y grupo control (C). Los animales del ECV tuvieron libre acceso a la rueda de carrera voluntaria, mientras que los del ECF fueron sometidos a carrera forzada en cinta sin fin (18 m/min, 0 por ciento inclinación, 60 m/min, 5 días/sem) durante ocho semanas. Fragmentos de los ventrículos izquierdo (VI) y derecho (VD) se recolectaron para análisis de los niveles de Hsp72. RESULTADOS: Las ratas del grupo ECV corrieron, en promedio 4,87 km, y las del ECF, 4,88 km por semana. Los animales de los grupos ECV y ECF ganaron menos peso (p<0,05) que los del grupo C (81,67 ± 11,95 g vs. 81,17 ± 10,18 g vs. 111,50 ± 2,26 g, respectivamente). El peso relativo del corazón no fue diferente (p>0,05) entre los grupos ECV, ECF y C (4,54 ± 0,79 mg/g vs. 4,94 ± 0,89 mg/g vs. 4,34 ± 0,87 mg/g, respectivamente). Las ratas entrenadas con carrera presentaron niveles de Hsp72 mayores (p<0,05) que las que corrieron voluntariamente, en el VI (287,45 ± 35,86 por ciento vs. 135,59 ± 5,10 por ciento, respectivamente) y en el VD (241,31 ± 25,83 por ciento vs. 137,91 ± 45,20 por ciento, respectivamente). CONCLUSIÓN: Los programas de entrenamiento con carreras voluntaria y forzada inducen niveles distintos de expresión de Hsp72 en el miocardio de ratas Wistar.

Different levels of Hsp72 in female rat myocardium in response to voluntary exercise and forced exercise.

BACKGROUND: Physical exercise induces hemodynamic stress. OBJECTIVE: To evaluate if voluntary running and forced running induced different levels of stress protein (Hsp72) in the myocardium of female Wistar rats. METHODS: Female rats were randomly assigned to the following groups: forced treadmill running group (FR; n= 6), voluntary running group (VR; n=6) and control group (C; n=6). VR group animals had free access to running wheels, and those from FR group underwent a running program on a treadmill (18 m/min, 60 min/day, 5 days/wk) for 8 weeks. Left ventricle (LV) and right ventricle (RV) fragments were collected at sacrifice, and the relative immunoblot contents of stress protein (Hsp72) were determined. RESULTS: VR animals ran on average 4.87 km/wk, and FR rats ran 4.88 km/wk. Animals from VR and FR groups had less body weight gain (p<0.05) than those from C group (81.67 +/- 11.95g vs 81.17 +/- 10.18g vs 111.50 +/- 2.26g, respectively). Heart weight/body weight ratio was not significantly different (p>0.05) among VR, FR and C groups (4.54 +/- 0.79 mg/g vs 4.94 +/- 0.89 mg/g vs 4.34 +/- 0.87 mg/g, respectively). FR group animals had levels of Hsp72 (p<0.05) higher than those from VR, both in LV (287.45 +/- 35.86 % vs 135.59 +/- 5.10 %, respectively) and RV (241.31 +/- 25.83 % vs 137.91 +/- 45.20 %, respectively). CONCLUSION: Voluntary running and forced running induced different levels of Hsp72 in the myocardium of female Wistar rats.