Exercise-induced Modulation of Extracellular Vesicles’ Cargo: a Focus on Antioxidants, Stress Proteins and miRNAs

2020 ◽  
Vol 159 ◽  
pp. S26
Author(s):  
Veronica Lisi ◽  
Chantalle Moulton ◽  
Ambra Antonioni ◽  
Cristina Fantini ◽  
Elisa Grazioli ◽  
...  
Keyword(s):  
Extracellular Vesicles ◽  
Stress Proteins ◽  
Exercise Induced

scholarly journals Exhaustive acute exercise-induced ER stress is attenuated in IL-6-knockout mice

2019 ◽  
Vol 240 (2) ◽  
pp. 181-193 ◽  
Author(s):  
Ana P Pinto ◽  
Alisson L da Rocha ◽  
Eike B Kohama ◽  
Rafael C Gaspar ◽  
Fernando M Simabuco ◽  
...  
Keyword(s):  
Physical Exercise ◽  
Er Stress ◽  
Knockout Mice ◽  
Acute Exercise ◽  
Stress Proteins ◽  
Serum Levels ◽  
Exercise Protocol ◽  
Caspase 12 ◽  
Exercise Induced ◽  
Eif2 Alpha

The endoplasmic reticulum (ER) stress and inflammation relationship occurs at different levels and is essential for the adequate homeostatic function of cellular systems, becoming harmful when chronically engaged. Intense physical exercise enhances serum levels of interleukin 6 (IL-6). In response to a chronic exhaustive physical exercise protocol, our research group verified an increase of the IL-6 concentration and ER stress proteins in extensor digitorium longus (EDL) and soleus. Based on these results, we hypothesized that IL-6-knockout mice would demonstrate a lower modulation in the ER stress proteins compared to the wild-type mice. To clarify the relationship between exercise-induced IL-6 increased and ER stress, we studied the effects of an acute exhaustive physical exercise protocol on the levels of ER stress proteins in the skeletal muscles of IL-6-knockout (KO) mice. The WT group displayed a higher exhaustion time compared to the IL-6 KO group. After 1 h of the acute exercise protocol, the serum levels of IL-6 and IL-10 were enhanced in the WT group. Independent of the experimental group, the CHOP and cleaved caspase 12/total caspase 12 ratio in EDL as well as ATF6 and CHOP in soleus were sensitive to the acute exercise protocol. Compared to the WT group, the oscillation patterns over time of BiP in EDL and soleus as well as of peIF2-alpha/eIF2-alpha ratio in soleus were attenuated for the IL-6 KO group. In conclusion, IL-6 seems to be related with the ER stress homeostasis, once knockout mice presented attenuation of BiP in EDL and soleus as well as of pEiF2-alpha/EiF2-alpha ratio in soleus after the acute exhaustive physical exercise protocol.

scholarly journals Significant increase in the secretion of extracellular vesicles and antibiotics resistance from methicillin-resistant Staphylococcus aureus induced by ampicillin stress

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Si Won Kim ◽  
Jong-Su Seo ◽  
Seong Bin Park ◽  
Ae Rin Lee ◽  
Jung Seok Lee ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Extracellular Vesicles ◽  
Stress Proteins ◽  
Stress Condition ◽  
Antibiotics Resistance ◽  
Stressed Condition ◽  
Cell Of Origin ◽  
First Line ◽  
Methicillin Resistant ◽  
Proteomic Approach

AbstractExtracellular vesicles (EVs) containing specific cargo molecules from the cell of origin are naturally secreted from bacteria. EVs play significant roles in protecting the bacterium, which can contribute to their survival in the presence of antibiotics. Herein, we isolated EVs from methicillin-resistant Staphylococcus aureus (MRSA) in an environment with or without stressor by adding ampicillin at a lower concentration than the minimum inhibitory concentration (MIC). We investigated whether EVs from MRSA under stress condition or normal condition could defend susceptible bacteria in the presence of several β-lactam antibiotics, and directly degrade the antibiotics. A comparative proteomic approach was carried out in both types of EVs to investigate β-lactam resistant determinants. The secretion of EVs from MRSA under antibiotic stressed conditions was increased by 22.4-fold compared with that of EVs without stress. Proteins related to the degradation of β-lactam antibiotics were abundant in EVs released from the stressed condition. Taken together, the present data reveal that EVs from MRSA play a crucial role in the survival of β-lactam susceptible bacteria by acting as the first line of defense against β-lactam antibiotics, and antibiotic stress leads to release EVs with high defense activity.

Etiology of Exercise-Induced Muscle Damage

1999 ◽  
Vol 24 (3) ◽  
pp. 234-248 ◽  
Author(s):  
Priscilla M. Clarkson ◽  
Stephen P. Sayers
Keyword(s):  
Muscle Damage ◽  
Eccentric Exercise ◽  
Muscle Function ◽  
Stress Proteins ◽  
Repair Process ◽  
Cellular Level ◽  
Muscle Stiffness ◽  
Damage Repair ◽  
Exercise Induced ◽  
Shock Proteins

Muscle damage is caused by strenuous and unaccustomed exercise, especially exercise involving eccentric muscle contractions, where muscles lengthen as they exert force. Damage can be observed both directly at the cellular level and indirectly from changes in various indices of muscle function. Several mechanisms have been offered to explain the etiology of the damage/repair process, including mechanical factors such as tension and strain, disturbances in calcium homeostasis. the inflammatory response, and the synthesis of stress proteins (heat shock proteins). Changes in muscle function following eccentric exercise have been observed at the cellular level as an impairment in the amount and action of transport proteins for glucose and lactate/H+, and at the systems level as an increase in muscle stiffness and a prolonged loss in the muscle's ability to generate force. This paper will briefly review factors involved in the damage/repair process and alterations in muscle function following eccentric exercise. Key words: eccentric exercise, inflammation, stress proteins, muscle function

scholarly journals Exercise and the Cardiovascular System

2012 ◽  
Vol 2012 ◽  
pp. 1-15 ◽  
Author(s):  
Saeid Golbidi ◽  
Ismail Laher
Keyword(s):  
Cardiovascular Disease ◽  
Stress Proteins ◽  
Lifestyle Modifications ◽  
Fat Reduction ◽  
Exercise Induced ◽  
Shock Proteins ◽  
Induced Changes ◽  
Main Effects ◽  
Mitochondrial Adaptation

There are alarming increases in the incidence of obesity, insulin resistance, type II diabetes, and cardiovascular disease. The risk of these diseases is significantly reduced by appropriate lifestyle modifications such as increased physical activity. However, the exact mechanisms by which exercise influences the development and progression of cardiovascular disease are unclear. In this paper we review some important exercise-induced changes in cardiac, vascular, and blood tissues and discuss recent clinical trials related to the benefits of exercise. We also discuss the roles of boosting antioxidant levels, consequences of epicardial fat reduction, increases in expression of heat shock proteins and endoplasmic reticulum stress proteins, mitochondrial adaptation, and the role of sarcolemmal and mitochondrial potassium channels in the contributing to the cardioprotection offered by exercise. In terms of vascular benefits, the main effects discussed are changes in exercise-induced vascular remodeling and endothelial function. Exercise-induced fibrinolytic and rheological changes also underlie the hematological benefits of exercise.

scholarly journals Exercise‐induced Extracellular Vesicles’ Effect on Stress.

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Kyeong Jin Yoon ◽  
Hae-Sung Cho ◽  
WonSang Lee ◽  
HyoYoul Moon
Keyword(s):  
Extracellular Vesicles ◽  
Exercise Induced

scholarly journals Effects of Voluntary Running Wheel Exercise-Induced Extracellular Vesicles on Anxiety

2021 ◽  
Vol 14 ◽  
Author(s):  
Kyeong Jin Yoon ◽  
Suhong Park ◽  
Seung Hee Kwak ◽  
Hyo Youl Moon
Keyword(s):  
Anxiety Disorders ◽  
Extracellular Vesicles ◽  
Neuronal Development ◽  
Cortical Cell ◽  
Field Tests ◽  
Voluntary Exercise ◽  
Receptor Interaction ◽  
Control Group ◽  
Running Wheel Exercise ◽  
Exercise Induced

Anxiety disorders are the most frequently diagnosed psychological condition, associated with serious comorbidities including excessive fear and interference with daily life. Drugs for anxiety disorders are typically prescribed but the side effects include weight gain, nausea, and sleepiness. Exercise is an effective treatment for anxiety. Exercise induces the release of extracellular vesicles (EVs) into the circulation, which transmit signals between organs. However, the effects of exercise-induced EVs on anxiety remain poorly understood. Here, we isolated EVs from the sera of mice that were sedentary or that voluntarily exercised. We characterized the changes in the miRNA profile of serum EVs after 4 weeks of voluntary exercise. miRNA sequencing showed that 82 miRNAs (46 of which were positive and 36 negative regulators) changed after exercise. We selected genes affected by at least two miRNAs. Of these, 27.27% were associated with neurotrophin signaling (9.09% with each of central nervous system neuronal development, cerebral cortical cell migration, and peripheral neuronal development). We also analyzed behavioral changes in mice with 3 weeks of restraint stress-induced anxiety after injection of 20 μg amounts of EVs from exercised or sedentary mice into the left cerebral ventricle. We found that exercise-derived EVs reduced anxiety (compared to a control group) in a nest-building test but found no between-group differences in the rotarod or open field tests. Exercise-derived EVs enhanced the expression of neuroactive ligand-receptor interaction genes. Thus, exercise-derived EVs may exhibit anti-anxiety effects and may be of therapeutic utility.

scholarly journals Molecular Mechanisms in Exercise-Induced Cardioprotection

2011 ◽  
Vol 2011 ◽  
pp. 1-15 ◽  
Author(s):  
Saeid Golbidi ◽  
Ismail Laher
Keyword(s):  
Molecular Mechanisms ◽  
Stress Proteins ◽  
Katp Channels ◽  
Behavioral Risk ◽  
No Production ◽  
Protective Mechanisms ◽  
Partial List ◽  
Exercise Induced ◽  
Improved Function ◽  
Shock Proteins

Physical inactivity is increasingly recognized as modifiable behavioral risk factor for cardiovascular diseases. A partial list of proposed mechanisms for exercise-induced cardioprotection include induction of heat shock proteins, increase in cardiac antioxidant capacity, expression of endoplasmic reticulum stress proteins, anatomical and physiological changes in the coronary arteries, changes in nitric oxide production, adaptational changes in cardiac mitochondria, increased autophagy, and improved function of sarcolemmal and/or mitochondrial ATP-sensitive potassium channels. It is currently unclear which of these protective mechanisms are essential for exercise-induced cardioprotection. However, most investigations focus on sarcolemmal KATP channels, NO production, and mitochondrial changes although it is very likely that other mechanisms may also exist. This paper discusses current information about these aforementioned topics and does not consider potentially important adaptations within blood or the autonomic nervous system. A better understanding of the molecular basis of exercise-induced cardioprotection will help to develop better therapeutic strategies.

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