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Jeongin Son J Son, Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, United States

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Jacob T. Bailey J Bailey, Department of Immunology and Microbial Disease, Albany Medical College, Albany, United States

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Stephen Worrell S Worrell, University of Pittsburgh School of Medicine, Pittsburgh, United States

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Adam B. Glick A Glick, Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, United States

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UV irradiation of the skin induces photo damage and generates cytotoxic intracellular reactive oxygen species (ROS), activating the unfolded protein response (UPR) to adapt or reduce these UVB-mediated damages. We previously identified a role for the key UPR mediator inositol requiring enzyme 1 (IRE1α) in the UV-DNA damage response. Here, we show that in the absence of IRE1α, PERK activity and protein levels are significantly compromised following UVB irradiation. Additionally, the loss of IRE1α suppressed phosphorylation of the PERK target, nuclear factor erythroid-2-related factor 2 (NRF2), and NRF2-dependent antioxidant gene expression after UVB irradiation. Interestingly, IRE1α-deficient keratinocytes exhibit elevated basal ROS levels, while a robust ROS induction upon UVB exposure is abolished. Because UVB-induced ROS plays an essential role in regulating skin inflammation, we analyzed recruited immune cell populations and the expression of pro-inflammatory cytokines, Il-6 and Tnfα in mice with epidermally-targeted deletion of Ire1α. Following UVB irradiation, there was significantly less recruitment of neutrophils and leukocytes and reduced expression of pro-inflammatory cytokine genes in the skin of mice lacking IRE1α. Furthermore, keratinocyte proliferation was also significantly reduced after chronic UVB exposure in the skin of these mice. Collectively, our findings indicate that IRE1α is essential for basal and UVB-induced oxidative stress response, UV-induced skin immune responses, and keratinocyte proliferation. These findings shed new light on the protective function of IRE1α in the response to UV.

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Josh Thorley J Thorley, School of sport, health, and exercise sciences, Loughborough University, Loughborough, LE11 3TU, United Kingdom of Great Britain and Northern Ireland

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Abrar Alhebshi A Alhebshi, Loughborough University, Loughborough, United Kingdom of Great Britain and Northern Ireland

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Stephen J. Bailey S Bailey, Loughborough University, Loughborough, United Kingdom of Great Britain and Northern Ireland

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Neil R.W Martin N Martin, Loughborough University, Loughborough, United Kingdom of Great Britain and Northern Ireland

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Nicolette C. Bishop N Bishop, Loughborough University, Loughborough, United Kingdom of Great Britain and Northern Ireland

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Tom Clifford T Clifford, Loughborough University, Loughborough, LE11 3TU, United Kingdom of Great Britain and Northern Ireland

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Objective:

To evaluate whether exercise induces different nuclear factor erythroid 2-related factor 2 (NRF2) responses in males and females Methods: 22 males and females (mean [SD]: age: 25 [6] years, height: 1.71 [0.10] m, weight: 69.6 [12.3] kg) performed 100 drop jumps and 50 squat jumps. NRF2/antioxidant response element (ARE) binding in peripheral blood mononuclear cells, glutathione peroxidase (GPX) activity, and immune markers influenced by NRF2 (interleukin-6 [IL-6], tumour necrosis factor-α [TNF-α], matrix metalloproteinase-9 [MMP-9], vascular cell adhesion molecule-1 [VCAM-1], total leukocytes, neutrophils, monocytes) were measured pre-, post-, and 1 h post-exercise.

Results:

NRF2/ARE binding did not significantly alter following exercise (p=0.59) and there were no sex differences (p=0.17). Similarly, GPX activity did not change post-exercise (p=0.74) and did not differ between sexes (p=0.61). IL-6 and TNF-α did not increase post-exercise (p>0.05 for both) but were lower in females (p<0.01 for both). MMP-9 increased post-exercise (p=0.02), but no group differences were found (p=0.27). VCAM-1 was unchanged after exercise (p=0.38) and did not differ between groups (p=0.11). Total leukocytes, neutrophil, and monocytes all increased post-exercise (p<0.01 for all); neutrophils were lower (p<0.01), and monocytes higher (p=0.03) in females vs. males.

Conclusion:

There were no sex differences in NRF2 activity at rest and in response to an exercise bout, however, several immune markers displayed sex-specific differences, independent to NRF2.

Significance: Sex differences in NRF2 signalling were not evident, suggesting males and females may incur similar redox-specific adaptations post-exercise.

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Roopak Murali Department of Human Genetics, Faculty of Biomedical Sciences, Technology and Research, Sri Ramachandra Institute of Higher Education and Research (SRIHER), Porur, Chennai, India

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Rachel Evangelina Department of Human Genetics, Faculty of Biomedical Sciences, Technology and Research, Sri Ramachandra Institute of Higher Education and Research (SRIHER), Porur, Chennai, India

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Joanna Pauline Samuel Department of Human Genetics, Faculty of Biomedical Sciences, Technology and Research, Sri Ramachandra Institute of Higher Education and Research (SRIHER), Porur, Chennai, India

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Pooja Singh Department of Human Genetics, Faculty of Biomedical Sciences, Technology and Research, Sri Ramachandra Institute of Higher Education and Research (SRIHER), Porur, Chennai, India

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Shivangi Saha Department of Plastic, Reconstructive and Burns Surgery, All India Institute of Medical Sciences (AIIMS), New Delhi, India

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Maneesh Singhal Department of Plastic, Reconstructive and Burns Surgery, All India Institute of Medical Sciences (AIIMS), New Delhi, India

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Rajesh Kumar Gandhirajan Department of Human Genetics, Faculty of Biomedical Sciences, Technology and Research, Sri Ramachandra Institute of Higher Education and Research (SRIHER), Porur, Chennai, India

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Graphical abstract

Abstract

Chronic wounds take longer to heal and, if left untreated, can result in severe repercussions such as sepsis, gangrene, and amputation. The current treatment procedures followed are wound cleaning and debridement, specialized dressings, antibiotics and antiseptics, hyperbaric oxygen therapy, and vacuum-assisted wound closure. Some of the limitations of these treatment options are multidrug resistance and tissue toxicity. Cold plasma is an emerging technology that has opened a new frontier in biomedical applications and is found to have great utility in wound healing. Cold plasma comprises reactive oxygen and nitrogen species (RONS) that can be targeted against bacterial inactivation and improve wound healing. The amount of RONS produced can be controlled by several parameters such as gas composition, flow rate, power, frequency, voltage, distance, and exposure time. The reactive species causes damage to the cell membrane as well as the intracellular components which ultimately lead to bacterial cell death. It can also accelerate wound healing by activating neutrophils, macrophages, endothelial cells, keratinocytes, and fibroblasts. These help in maintaining tissue oxygenation, initiating angiogenesis, collagen synthesis which aids in rapid wound closure. In this review, we summarize the various characteristics of cold plasma that can be optimized to produce an effective antimicrobial effect. The different mechanisms of bacterial inactivation and the stimulation of wound healing processes by the reactive species are discussed. Furthermore, numerous pieces of evidence from in vitro and in vivo experiments and clinical trials that prove that cold plasma is an effective approach are presented.

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Irene Martín-Bocanegra Institute of Biomedicine of Seville (IBiS), Hospital University Virgen del Rocío/CSIC/University of Seville, Seville, Spain

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Thaissa Horne Institute of Biomedicine of Seville (IBiS), Hospital University Virgen del Rocío/CSIC/University of Seville, Seville, Spain

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Belén Maqueda-Hernández Institute of Biomedicine of Seville (IBiS), Hospital University Virgen del Rocío/CSIC/University of Seville, Seville, Spain

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Elena Navarro-Villarán Institute of Biomedicine of Seville (IBiS), Hospital University Virgen del Rocío/CSIC/University of Seville, Seville, Spain
Department of Medical Physiology and Biophysics, University of Seville, Seville, Spain

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Jordi Muntané Institute of Biomedicine of Seville (IBiS), Hospital University Virgen del Rocío/CSIC/University of Seville, Seville, Spain
Department of Medical Physiology and Biophysics, University of Seville, Seville, Spain
Biomedical Research Center for Hepatic and Digestive Diseases (CIBERehd), Madrid, Spain

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The mammalian target of rapamycin (mTOR) is a master regulator of the cell metabolism which impacts numerous signaling involved in cell proliferation and death and recycling cell constituents to readapt to new physiological or pathological environments. mTOR is constituted by two structural and functional different complexes, mTORC1 and mTORC2. Both can be independently regulated, which has a great impact on the effectiveness of therapeutic interventions in different clinical and experimental situations. Furthermore, mTORC1 interacts with specific chaperones or immunophilins which are intracellular receptors of the immunosuppressive drugs. Low and high molecular weights of immunophilins have different intracellular functions. The present review updates the molecular structure and signaling of mTOR as well as their regulation by immunophilins and upstream and downstream signaling events, highlighting the potential therapeutic intervention of mTOR in cancer, metabolic disturbances, and aging.

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Elena Cavallone Division of Cardiology, San Luigi Gonzaga University Hospital, Orbassano, Turin, Italy
Division of Cardiology, Department of Medical Sciences, University of Turin, Italy

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Amir Hassan Mousavi Division of Cardiology, San Luigi Gonzaga University Hospital, Orbassano, Turin, Italy

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Carloalberto Biolé Division of Cardiology, San Luigi Gonzaga University Hospital, Orbassano, Turin, Italy

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Giulia Nangeroni Division of Cardiology, San Luigi Gonzaga University Hospital, Orbassano, Turin, Italy

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Alessandra Chinaglia Division of Cardiology, San Luigi Gonzaga University Hospital, Orbassano, Turin, Italy

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Matteo Bianco Division of Cardiology, San Luigi Gonzaga University Hospital, Orbassano, Turin, Italy

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Heart failure is a progressive disease, representing a growing cause of morbidity, hospitalization, and mortality. An increasingly common type of heart failure with preserved ejection fraction (HFpEF) is an immunoglobulin light chain and transthyretin cardiac amyloidosis, in the pathophysiology of which oxidative damage appears to exert a strong impact. Reactive oxygen and nitrogen species have physiological signaling functions, but their overaccumulation, as in cardiac amyloidosis, leads to cardiomyocyte damage and apoptosis, and to cardiac hypertrophy and fibrosis. Moreover, such pathological processes worsen the redox damage with the perpetuation of an inflammatory state, in a vicious cycle. Here, the role of oxidative damage in the transthyretin and immunoglobulin light chain cardiac amyloidosis, the underlying pathogenic mechanisms, the therapeutic implications, and possible future strategies are reviewed.

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Tania Medali Biological Adaptation and Ageing (B2A), CNRS UMR-8256/INSERM ERL U-1164, Biological Institute Paris-Seine, Sorbonne University, Paris, France

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Dominique Couchie Biological Adaptation and Ageing (B2A), CNRS UMR-8256/INSERM ERL U-1164, Biological Institute Paris-Seine, Sorbonne University, Paris, France

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Nathalie Mougenot Plateforme PECMV, UMS28 INSERM, Faculté de Médecine, Sorbonne University, Paris, France

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Maria Mihoc Plateforme PECMV, UMS28 INSERM, Faculté de Médecine, Sorbonne University, Paris, France

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Olaf Bergmann Department of Cell and Molecular Biology, Karolinska Institute, Stockholm, Sweden CRTD, TU Dresden, Dresden, Germany

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Wouter Derks Department of Cell and Molecular Biology, Karolinska Institute, Stockholm, Sweden CRTD, TU Dresden, Dresden, Germany

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Celio X Santos BHF Centre of Excellence King's College London, The James Black Centre, London, UK

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Bertrand Friguet Biological Adaptation and Ageing (B2A), CNRS UMR-8256/INSERM ERL U-1164, Biological Institute Paris-Seine, Sorbonne University, Paris, France

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Mustapha Rouis Biological Adaptation and Ageing (B2A), CNRS UMR-8256/INSERM ERL U-1164, Biological Institute Paris-Seine, Sorbonne University, Paris, France

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Graphical abstract

Experimental Myocardial infarction (MI) using ligation procedure induces cardiac dysfunction, high level of ROS, inflammation, apoptosis, fibrosis and cardiomyocyte (CM) loss. AAV overexpressing human Trx-2, specifically in CM mitochondria improves mouse cardiac function, reduces the size of cardiac infarct, increases the expression of cardiac anti-inflammatory markers, reduces apoptosis and oxidative stress. However, it does not increase CM proliferation.

Abstract

Introduction and objective

Myocardial infarction (MI), which in general results from complications of atherosclerosis, is characterized by high inflammation and cardiomyocytes (CMs) apoptosis and by major loss of CMs. Regeneration of these lost CMs represents a major challenge for MI therapy. The increase of mitochondrial reactive oxygen species (ROS) is involved in cell cycle arrest which can be restarted by hypoxia or in the presence of ROS scavengers. Among ROS scavengers, mitochondrial thioredoxin 2 (Trx-2), an important antioxidant protein, could play a role in the CMs renewal.

Method

In this study, we investigated the effect of Trx-2 on mouse heart after an experimental MI.

Results

Trx-2 improves mouse cardiac function, reduces cardiac infarction size and increases the expression of cardiac anti-inflammatory markers. In addition, it reduces apoptosis and oxidative stress in heart tissue of mice after MI but it does not increase CM proliferation in cell culture or in heart tissue.

Conclusion

Mitochondrial Trx-2 effectively protects against heart infarction, likely via the reduction of oxidative stress, inflammation and apoptosis but not through CM renewal.

Significance statement

The current study unveils the complexities of MI and highlights mitochondrial Trx-2 role. Post-MI, marked by inflammation, CM apoptosis and significant CM loss. Trx-2 emerges as a vital protector. Its intervention improves mouse cardiac function, reduces infarction size and fosters an anti-inflammatory environment. By uncovering these mechanisms, the study suggests potential therapeutic strategies for oxidative stress, inflammation and apoptosis in MI, positioning Trx-2 as a promising candidate for future cardiac interventions.

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Cristina Russo Section of Pathology, Department of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy

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Maria Stella Valle Section of Physiology, Department of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy

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Lucia Malaguarnera Section of Pathology, Department of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy

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Graphical abstract

Abstract

Pathological conditions characterized by systemic inflammation and oxidative stress can often impair the muscle cells efficiency. The gradual decline of muscle mass and tone drastically reduces the motor skills of the patient affecting the simplest daily activities. Muscle dysfunction, resulting in the deterioration of muscle tissue, can lead to a serious situation of muscle wasting that can evolve into sarcopenia. In addition, muscle dysfunction causing metabolic disorders impairs the quality of life. The function of skeletal muscle is deeply conditioned by environmental, nutritional, physical, and genetic factors. Proper nutrition with balanced protein and vitamins intake and an active lifestyle helps to strengthen tissues and counteract pathological conditions and generalized weakness. Vitamin D performs antioxidant actions, indispensable in skeletal muscle. Epidemiological data indicate that vitamin D deficiency is a widespread status in the world. Vitamin D deficiency induces mitochondrial failure, reduced production of adenosine triphosphate, oxidative injury, and compromised muscle function. Among the different types of antioxidants, vitamin D has been identified as the main compound that can improve the effectiveness of the treatment for muscle weakness and improve conditions related to sarcopenia. The purpose of this review is to analyze molecular processes used by vitamin D against oxidative stress and how it can affect muscle function in order to assess whether its use as a supplement in inflammatory pathologies and oxidative stress can be useful to prevent deterioration and improve/maintain muscle function.

Open access
Daniela Weber Department of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), Nuthetal, Germany
Food4Future (F4F), c/o Leibniz Institute of Vegetable and Ornamental Crops (IGZ), Grossbeeren, Germany
NutriAct Competence Cluster Nutrition Research Berlin-Potsdam, Nuthetal, Germany

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Tilman Grune Department of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), Nuthetal, Germany
Food4Future (F4F), c/o Leibniz Institute of Vegetable and Ornamental Crops (IGZ), Grossbeeren, Germany
NutriAct Competence Cluster Nutrition Research Berlin-Potsdam, Nuthetal, Germany
Institute of Nutritional Science, University of Potsdam, Potsdam, Germany
Department of Physiological Chemistry, Faculty of Chemistry, University of Vienna, Vienna, Austria

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The aim of this review is to provide a comprehensive and simple graphical overview on carotenoids. The review describes in four detailed figures the course of carotenoids from food to skin. Differences in chemical structures of the six most prominent carotenoids, namely, α-carotene, β-carotene, lutein, zeaxanthin, lycopene and β-cryptoxanthin, and their seasonal variations in plasma concentrations resulting from different availability of fruits and vegetables are highlighted. Furthermore, factors affecting carotenoid status, sites of storage and how and where they can be assessed (dietary intake and in vivo) are discussed. The route of carotenoid transport after ingestion, transport across the enterocyte and receptors involved in carotenoid uptake in peripheral cells are shown followed by the routes of carotenoid delivery to the skin and reasons for variations in skin carotenoid status are visualized.

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Maret G Traber Linus Pauling Institute, Oregon State University, Corvallis, Oregon, USA

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This is a narrative review of the evidence of α-tocopherol importance in human health, especially with regards to its vitamin role. α-Tocopherol is a potent peroxyl radical scavenger, and this role is prominent in its efficacy in maintaining the metabolic health of tissues. Vitamin E deficiency is discussed as a tool to understand the impact of α-tocopherol’s absence promoting increased lipid peroxidation and polyunsaturated fatty acid depletion. Downstream deficiency consequences include impacts on choline and one-carbon metabolism, glucose and energy metabolism, and their interactions with critical thiols, such as glutathione. Importantly, human vitamin E deficiency, caused by genetic defects in the α-tocopherol transfer protein (α-TTP), provides important clues for the necessity of α-tocopherol for the peripheral nervous system. Moreover, α-TTP expression in the liver, brain, eyes, and placenta illustrates that these tissues are especially vulnerable and require this specific α-tocopherol delivery mechanism for their protection. Although clinical trial evidence is limited and equivocal about the health benefits of vitamin E supplements, there is epidemiologic evidence of the long-term benefits of increased α-tocopherol intakes in ’healthy’ diets (high in vegetables and fruits, fish, nuts, and seeds, as well as fiber).

Significance statement

The elaborate regulation of α-tocopherol concentrations by the human body suggests that the consistent consumption of the recommended amounts of dietary α-tocopherol (15 mg) over a lifetime are protective of the at-risk tissues, as well as providing protection from chronic diseases.

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