Cell Growth & Mitochondrial Function: Where Music Stands
News Release, World Mitochondria Society, Berlin - Germany – March 25, 2022
Mitochondria are considered a portal to receive, process and integrate external energy and information to maintain cellular homeostasis. Previous studies demonstrated that mitochondrial function and antioxidant capacity of in-vitro cultured mammalian cells is modified by different energetic stimuli including electromagnetic energy, acoustic energy, external Qi and subtle energy emitted by written texts in relatively short time frames. Thus, individual cells can act as a rapid and sensitive biological sensor and act as a platform to evaluate and understand the subtle effect of different biophysical stimuli.
Regarding acoustic energy, several different types of music have been reported to produce beneficial effects on human health. Feng et al, compared eastern and western music styles on cell function at the biochemical level to understand the underlying mechanisms involved.
They compared the effects of Chinese five-element music with two types of western music (heavy-metal and classical) on mitochondrial function, oxidative capacity and growth using human embryonic kidney cells (HEK293T cells).
Exposing cells to five-element music produced several beneficial physiological effects including:
- Increases in the production of adenosine triphosphate (ATP) by 17%, glutathione (GSH) by 21% and cell growth rates by 14%
- Significant reduction in the reactive oxygen species (ROS) by 13%.
The group treated with classical music:
- There was only a trend toward increased GSH (8%), although the increased growth rates (14%) did reach significance.
Cells treated with heavy-metal music responded oppositely:
- Significant 16% increase in ROS
- Significant 11% reduction in cell viability
This study revealed dramatically different effects of different styles of music on specific biochemical measures in cultured human cells. It helped explain the underlying biochemical mechanisms of the effects of the different types of music.
Targeting Mitochondria 2022 will introduce to the most recent discoveries on mitochondria. Join us this October and be up to date with all the new research in this field.
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Delivery of Mitochondria via Extracellular Vesicles: A New Horizon in Drug Delivery
News Release, World Mitochondria Society, Berlin - Germany – March 23, 2022
Extracellular vesicles (EVs) have been well reported to mediate intercellular communication and carry a rich cocktail of innate cargo including lipids, proteins and nucleic acids.
Keeping in mind, the field of drug delivery has made tremendous advances in increasing the therapeutic potential of a variety of drug candidates spanning from small molecules to large molecular biologics such as nucleic acids, proteins, etc. EVs are a promising class of natural, cell-derived carriers for drug delivery.
EVs of particle diameters <200 nm are referred to as small EVs (sEVs) and medium-to-larger particles of diameters >200 nm are referred to as m/lEVs. The m/lEVs naturally incorporate mitochondria during their biogenesis.
It has been established that mitochondrial damage and dysfunction play a causal role in multiple pathologies such as neurodegenerative diseases, cardiovascular and metabolic diseases—suggesting that m/lEV-mediated mitochondria delivery can be of broad biomedical significance.
In this brilliant review, Dr. Devika S.Manickam discusses the potential of m/lEVs as carriers for the delivery of healthy and functional mitochondria.
She states that a major advantage of harnessing m/lEVs is that the delivered mitochondria are capable of using endogenous mechanisms for repairing the cellular damage. She also highlights the delivery potential of m/lEVs based on the studies that have been conducted so far, and discusses unaddressed issues towards their development as a novel class of mitochondria carriers.
Dr. Manickam will be joining us in Targeting Mitochondria 2022 to give her talk within the "Extracellular Vesicles & Mitochondria: The Target" session. Register now for a chance to benefit from the exprience of professional speakers in this field.
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Exercise in Post-acute COVID-19 Syndrome Patients: Fatty Acid Oxidation & Lactate Production
News Release, World Mitochondria Society, Berlin - Germany – March 21, 2022
After acute infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), many individuals experience a range of symptoms including dyspnea, exercise intolerance, and chest pain commonly referred to as “post–COVID-19 syndrome” or as post-acute sequelae of SARS-CoV-2 infection (PASC). Exertional dyspnea and physical activity intolerance in PASC can be debilitating despite mild acute coronavirus disease (COVID-19) and normal resting pulmonary physiology and cardiac function.
There is an urgent need to understand the pathogenesis of PASC and find effective treatments. The cardiopulmonary exercise test (CPET) is commonly used to investigate unexplained exertional dyspnea; as such, it could provide insight into mechanisms of PASC. CPET data can be used to calculate rates of β-oxidation of fatty acids (FATox) and of lactate clearance, providing insight into mitochondrial function. Fit individuals have better mitochondrial function and a higher rate of FATox during exercise than less fit individuals. In this study, they investigated whether patients with PASC had compromised mitochondrial function during graded exercise.
Data were obtained via retrospective review of the electronic medical record from a cohort of 50 subjects with PASC that were consecutively referred to and willing to complete CPET in the Pulmonary Physiology Laboratory at National Jewish Health between June 2020 and April 2021. Patients were assessed on a cycle ergometer using a continuous ramp protocol to exhaustion. Cardiovascular, ventilatory, metabolic, and gas exchange data were collected using a metabolic cart (Ultima Cardio2 System; Med graphics) per standard protocol. As a final step, patient data were compared with results from two published cohorts that included subjects tested with CPET in Denver, Colorado.
- Pulmonary function testing (PFT) showed mostly normal resting airflow and gas transfer capacity. All six patients (12%) with PFT abnormalities had preexisting illnesses, including asthma (n = 3) or interstitial lung disease. Resting transthoracic echocardiogram was obtained in 39 patients (78%) within 2 ± 3 months of CPET.
- Left ventricular systolic function was normal in all patients. Among the 50 patients who underwent CPET, the mean time from COVID-19 diagnosis to the CPET was 6 ± 4 months.
- Regardless of the presence of comorbidities, among the 39 patients with PASC who had arterial catheters in place, mean lactate was significantly higher; and in all 50 patients with PASC, calculated levels of FATox were significantly lower during exercise when compared with historical cohorts of subjects who are moderately active or with metabolic syndrome.
The data suggest that abnormally low FATox and altered lactate production by skeletal muscle as a putative cause of / contributor to the functional limitation of patients with PASC.
Normally, as glycolysis increases with exercise intensity, lactate is oxidized for fuel in mitochondria, mainly in adjacent slow-twitch muscle fibers. Like FATox, lactate clearance capacity is a useful surrogate for mitochondrial function. In patients with PASC, even in those with normal pre–COVID-19 physical fitness and free of comorbidities, the metabolic disturbances of the skeletal muscle during exercise may be worse than those reported in moderately active individuals or in individuals with metabolic syndrome. Whereas rising blood lactate levels are expected during high exercise intensity (as glycolytic flux exceeds the rate of mitochondrial pyruvate oxidation), a high blood lactate at lower exercise levels indicates mitochondrial dysfunction. The inappropriately high arterial lactate levels at relatively low exercise intensity in patients with PASC indicate that the transition from FATox to CHOox occurs prematurely, suggesting metabolic reprogramming and dysfunctional mitochondria.
This study provides the first evidence of mitochondrial dysfunction that advances our understanding of the pathogenesis of PACS in patients with preserved pulmonary and cardiac function. Future studies into the mechanisms of mitochondrial dysfunction in individuals with PACS will help accelerate the development of therapies to improve their functional status.
The implication of mitochondria in COVID-19 pathogenesis will be highlighted in Targeting Mitochondria 2022. If you have any studies that fit this title, you can submit your abstract now and share your work with the world mitochondria society.
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Pleiotropic Effects of Mitochondria in Aging
News Release, World Mitochondria Society, Berlin - Germany – March 22, 2022
The mitochondrial stress-response (MSR) network contributes to the reconstitution of cellular homeostasis by preventing mitochondrial proteotoxicity and by redistributing and removing irreversibly damaged elements of the mitochondria. Recently, scientists have gained considerable insights into why a decline in the robustness of these MSR pathways contributes to cellular damage and organismal deterioration.
This study by Lima et al., published in nature aging, described the pleiotropic effects of mitochondrial dysfunction in aging.
Pleiotropic effects of mitochondria in aging
They outlined the major mitochondrial stress pathways, how their failure is interconnected with the expansion of mitochondrial DNA mutations and deregulated metabolism, and how this affects cellular and organismal homeostasis.
They furthermore provided an integrated map of how combined mitochondrial defects impact several features of aging, suggesting conserved links that could potentially be harnessed to slow the aging process. They described recent evidence arguing that defects in these conserved adaptive pathways contribute to aging and age-related diseases. Signaling pathways regulating the mitochondrial unfolded protein response, mitochondrial membrane dynamics, and mitophagy are discussed, emphasizing how their failure contributes to heteroplasmy and de-regulation of key metabolites.
The current understanding of how these processes are controlled and interconnected explains how mitochondria can widely impact fundamental aspects of aging.
Targeting Mitochondria 2022 will dedicate w whole session to Nuclear-Mitochondrial Interactions and their Effect on Longevity and Health. Professional speakers like Dr. Raghavan Pillai Raju will discuss the role of mitochondria in aging.
Don't miss out and register now.
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Sustained Killing by Cytotoxic T cells: Mitochondrial Role
News Release, World Mitochondria Society, Berlin - Germany – March 18, 2022
Cytotoxic T lymphocytes (CTLs) can terminate both virally infected cells and cancer cells by secreting cytolytic proteins such as perforin and granzyme B. Lisci et al. have identified mitochondria as important regulators of CTL killing; mice lacking the deubiquitinase USP30 have CTLs acutely depleted of mitochondria, and these cells have reduced killing ability but normal motility, signaling, and secretion.
Although mitochondrial mass has been correlated with CTL antitumor activity, CTLs show an increased reliance on glycolysis, suggesting a decreased dependence on mitochondrial respiration. Whether, how, or why mitochondria contribute as CTLs seek, recognize, and kill their targets is not well understood.
In this research, Lisci et al., generated CTLs from USP30-deficient mice to study the nature of this defect and to understand how it affects killing.
They reported the following:
T cell development was unaffected in USP30-deficient mice. However, upon activation, CD8+ T cells generated CTLs with an acute loss of mitochondria and impaired killing.
The cytotoxicity of USP30-deficient CTLs diminished with time, indicating a defect in sustained killing.
Despite the loss of mitochondria and decreased oxidative phosphorylation in Usp30−/− CTLs, motility, signaling, and secretion, which are required for killing, were all intact. However, the secretory granule size was reduced in Usp30−/− CTLs, with a reduction in newly synthesized intermediates of key cytolytic proteins, perforin and granzyme B. This suggested an underlying defect in the de novo protein synthesis, which is required for sustained killing.
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