scholarly journals Tissue-Specific Profiling of Oxidative Stress-Associated Transcriptome in a Healthy Mouse Model

2018 ◽  
Vol 19 (10) ◽  
pp. 3174 ◽  
Author(s):  
Jung Kim ◽  
Hyeong Kim ◽  
Chang Son
Keyword(s):  
Oxidative Stress ◽  
Quantitative Polymerase Chain Reaction ◽  
Specific Gene ◽  
Tissue Specific ◽  
Age Related ◽  
Wide Range ◽  
Liver And Kidney ◽  
Specific Variation ◽  
Polymerase Chain ◽  
Lung And Kidney

Oxidative stress is a common phenomenon and is linked to a wide range of diseases and pathological processes including aging. Tissue-specific variation in redox signaling and cellular responses to oxidative stress may be associated with vulnerability especially to age-related and chronic diseases. In order to provide a basis for tissue-specific difference, we examined the tissue-specific transcriptional features of 101 oxidative stress-associated genes in 10 different tissues and organs of healthy mice under physiological conditions. Microarray analysis results, which were consistent with quantitative polymerase chain reaction (qPCR) results, showed that catalase, Gpx3, and Gpx4 were most highly regulated in the liver, kidney, and testes. We also found the tissue-specific gene expression of SOD1 (liver and kidney), SOD2 (heart and muscle), and SOD3 (lung and kidney). The current results will serve as a reference for animal models and help advance our understanding of tissue-specific variability in oxidative stress-associated pathogenesis.

scholarly journals Stress reactivity elicits a tissue-specific reduction in telomere length in ageing zebrafish (Danio rerio)

2020 ◽  
Author(s):  
James R. Evans ◽  
Jose V. Torres-Pérez ◽  
Maria Elena Miletto Petrazzini ◽  
Riva Riley ◽  
Caroline H. Brennan
Keyword(s):  
Telomere Length ◽  
Stress Reactivity ◽  
Quantitative Polymerase Chain Reaction ◽  
Heart Tissue ◽  
Telomere Shortening ◽  
Tissue Specific ◽  
Age Related ◽  
Specific Manner ◽  
Polymerase Chain ◽  
The Relationship

ABSTRACTTelomere length reflects cellular ageing. Increased telomere shortening in leukocytes is associated with a range of neurodegenerative and cardiovascular diseases, the onset and progression of which may be mediated by behavioural traits such as anxiety and stress reactivity. However, the effects of the hypothalamus-pituitary-adrenal axis stress response are shown to be tissue specific. As such, leukocyte telomere length may not give an accurate measure of the relationship between stress-reactivity and telomere length in disease relevant tissues. To test the hypothesis that stress-reactivity contributes to age-related telomere shortening in a tissue specific manner, we examined the correlation between telomere length in heart and brain tissue and stress-reactivity in a population of young (6-9 month) and ageing (18 month) zebrafish. Stress-reactivity was assessed by tank diving, a zebrafish version of the rodent open-field test, and through gene expression. Telomere length was assessed using quantitative polymerase chain reaction. We show that ageing zebrafish have shorter telomeres in both heart and brain. Telomere length is inversely related to stress-reactivity in heart but not brain of ageing individuals. These data support the hypotheses that an anxious predisposition contributes to telomere shortening in heart tissue, and by extension age-related heart disease, and that stress-reactivity contributes to age-related telomere shortening in a tissue-specific manner.

PHYSICAL ACTIVITY AS HEALTHY INTERVENTION AGAINST SEVERE OXIDATIVE STRESS IN ELDERLY POPULATION

2013 ◽  
pp. 1-9
Author(s):  
C. TOMAS-ZAPICO ◽  
E. IGLESIAS-GUTIERREZ ◽  
B. FERNANDEZ-GARCIA ◽  
D. DE GONZALO-CALVO
Keyword(s):  
Oxidative Stress ◽  
Physical Activity ◽  
Elderly Population ◽  
Physiological Basis ◽  
Related Disease ◽  
Age Related ◽  
Wide Range ◽  
Health Related ◽  
Relevant Risk Factor

Severe oxidative stress is a relevant risk factor for major deleterious health-related events in olderpeople and is thought to be an important contributor to age-related disease. Literature has suggested oxidativestress as a therapeutic target for mitigating the biological decline and attenuating the occurrence of adverseclinical events in aged individuals. However, definitive treatments are not known. Regular and moderate physicalactivity has been proposed as possible intervention for slowing age-related decline. This healthy strategy presentsa wide range of beneficial aspects for elderly, from the reduction of morbidity, disability, frailty and mortalityrates to treatment of many age-related disorders. Importantly, the global benefits on health are not shared by anyother strategies. Nevertheless, the physiological basis by which exercise produces its benefits to the organism isnot fully understood. This review summarizes the evidence for the role of physical activity as potential healthyintervention for mitigating the negative aspects of aging through the modulation of the oxidative mechanisms.

scholarly journals Andrographis paniculata and Its Bioactive Diterpenoids Against Inflammation and Oxidative Stress in Keratinocytes

Antioxidants ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 530 ◽  
Author(s):  
Eugenie Mussard ◽  
Sundy Jousselin ◽  
Annabelle Cesaro ◽  
Brigitte Legrain ◽  
Eric Lespessailles ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Quantitative Polymerase Chain Reaction ◽  
Andrographis Paniculata ◽  
Ros Production ◽  
Inflammatory Conditions ◽  
Tnf Α ◽  
Dichlorofluorescein Diacetate ◽  
Polymerase Chain ◽  
Factor Α ◽  
Necrosis Factor

Andrographis paniculata was widely used in traditional herbal medicine to treat various diseases. This study explored the potential anti-aging activity of Andrographis paniculata in cutaneous cells. Human, adult, low calcium, high temperature (HaCaT) cells were treated with methanolic extract (ME), andrographolide (ANDRO), neoandrographolide (NEO), 14-deoxyandrographolide (14DAP) and 14-deoxy-11,12-didehydroandrographolide (14DAP11-12). Oxidative stress and inflammation were induced by hydrogen peroxide and lipopolysaccharide/TNF-α, respectively. Reactive oxygen species (ROS) production was measured by fluorescence using a 2′,7′-dichlorofluorescein diacetate (DCFH-DA) probe and cytokines were quantified by ELISA for interleukin-8 (IL-8) or reverse transcription-quantitative polymerase chain reaction (RT-qPCR) for tumor necrosis factor-α (TNF-α). Hyaluronic acid (HA) secretion was determined by an ELISA. Our results show a decrease in ROS production and TNF-α expression by ME (5 µg/mL) in HaCaT under pro-oxidant and pro-inflammatory conditions, respectively. ME protected HaCaT against oxidative stress and inflammation. Our findings confirm that ME can be used for the development of bioactive compounds against epidermal damage.

scholarly journals Neuroinflammation in Primary Open-Angle Glaucoma

2020 ◽  
Vol 9 (10) ◽  
pp. 3172 ◽  
Author(s):  
Stefania Vernazza ◽  
Sara Tirendi ◽  
Anna Maria Bassi ◽  
Carlo Enrico Traverso ◽  
Sergio Claudio Saccà
Keyword(s):  
Oxidative Stress ◽  
Immune Response ◽  
Trabecular Meshwork ◽  
Primary Open Angle Glaucoma ◽  
Open Angle Glaucoma ◽  
Glaucoma Surgery ◽  
Open Angle ◽  
Antioxidant Defences ◽  
Age Related ◽  
Wide Range

Primary open-angle glaucoma (POAG) is the second leading cause of irreversible blindness worldwide. Increasing evidence suggests oxidative damage and immune response defects are key factors contributing to glaucoma onset. Indeed, both the failure of the trabecular meshwork tissue in the conventional outflow pathway and the neuroinflammation process, which drives the neurodegeneration, seem to be linked to the age-related over-production of free radicals (i.e., mitochondrial dysfunction) and to oxidative stress-linked immunostimulatory signaling. Several previous studies have described a wide range of oxidative stress-related makers which are found in glaucomatous patients, including low levels of antioxidant defences, dysfunction/activation of glial cells, the activation of the NF-κB pathway and the up-regulation of pro-inflammatory cytokines, and so on. However, the intraocular pressure is still currently the only risk factor modifiable by medication or glaucoma surgery. This present review aims to summarize the multiple cellular processes, which promote different risk factors in glaucoma including aging, oxidative stress, trabecular meshwork defects, glial activation response, neurodegenerative insults, and the altered regulation of immune response.

scholarly journals Network propagation of rare variants in Alzheimer’s disease reveals tissue-specific hub genes and communities

2021 ◽  
Vol 17 (1) ◽  
pp. e1008517
Author(s):  
Marzia Antonella Scelsi ◽  
Valerio Napolioni ◽  
Michael D. Greicius ◽  
Andre Altmann ◽  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Rare Variants ◽  
Late Onset ◽  
Integrative Approach ◽  
Specific Gene ◽  
Tissue Specific ◽  
Association Testing ◽  
Wide Range ◽  
Network Propagation

State-of-the-art rare variant association testing methods aggregate the contribution of rare variants in biologically relevant genomic regions to boost statistical power. However, testing single genes separately does not consider the complex interaction landscape of genes, nor the downstream effects of non-synonymous variants on protein structure and function. Here we present the NETwork Propagation-based Assessment of Genetic Events (NETPAGE), an integrative approach aimed at investigating the biological pathways through which rare variation results in complex disease phenotypes. We applied NETPAGE to sporadic, late-onset Alzheimer’s disease (AD), using whole-genome sequencing from the AD Neuroimaging Initiative (ADNI) cohort, as well as whole-exome sequencing from the AD Sequencing Project (ADSP). NETPAGE is based on network propagation, a framework that models information flow on a graph and simulates the percolation of genetic variation through tissue-specific gene interaction networks. The result of network propagation is a set of smoothed gene scores that can be tested for association with disease status through sparse regression. The application of NETPAGE to AD enabled the identification of a set of connected genes whose smoothed variation profile was robustly associated to case-control status, based on gene interactions in the hippocampus. Additionally, smoothed scores significantly correlated with risk of conversion to AD in Mild Cognitive Impairment (MCI) subjects. Lastly, we investigated tissue-specific transcriptional dysregulation of the core genes in two independent RNA-seq datasets, as well as significant enrichments in terms of gene sets with known connections to AD. We present a framework that enables enhanced genetic association testing for a wide range of traits, diseases, and sample sizes.

scholarly journals Evaluation of toxicity and response to oxidative stress generated by orthodontic bands in human gingival fibroblasts

2019 ◽  
Vol 90 (2) ◽  
pp. 285-290 ◽  
Author(s):  
Alexandre Marcos Bandeira ◽  
Elizabeth Ferreira Martinez ◽  
Ana Paula Dias Demasi
Keyword(s):  
Oxidative Stress ◽  
Quantitative Polymerase Chain Reaction ◽  
Conditioned Media ◽  
Human Gingival Fibroblasts ◽  
Gingival Fibroblasts ◽  
Trypan Blue Exclusion ◽  
Antioxidant Genes ◽  
Glutathione Peroxidase 1 ◽  
Viable Cells ◽  
Polymerase Chain

ABSTRACT Objective: To evaluate the cytotoxicity of stainless-steel orthodontic bands and their influence on the expression of the antioxidant genes in human gingival fibroblasts. Materials and Methods: Ten bands of each brand (Dentsply-Sirona, Dentaurum, TP Orthodontics, and Morelli) were conditioned in 0.2 g/mL culture medium at 37°C for 14 days, and the corresponding conditioned media were applied over the fibroblasts. Cell viability was assessed after 24, 48, and 72 hours of exposure to the conditioned media by trypan blue exclusion assay. Expression of the antioxidant defense genes peroxiredoxin 1 (PRDX1), superoxide dismutase 1 (SOD1), and glutathione peroxidase 1 (GPX1) were evaluated by quantitative polymerase chain reaction after 24 hours of exposure. These parameters were compared to those of the cells not exposed to the conditioned media of the bands (control). Results: All bands promoted a reduction in the number of viable cells in the periods of 48 and 72 hours (P < .01). Analysis of gene expression showed a significant increase in the levels of PRDX1 transcripts caused by the conditioned media of the Dentsply-Sirona, TP Orthodontics, and Morelli bands (P < .01) as well as induction of SOD1 by the conditioned media of the Dentaurum and Morelli (P < .01). Expression of GPX1 was not influenced by the conditioned media. Conclusions: The orthodontic bands showed toxicity to fibroblasts and increased the expression of PRDX1 and SOD1 antioxidant genes, indicating induction of oxidative stress in the cells.

scholarly journals Redox-Dependent Structural Modification of Nucleoredoxin Triggers Defense Responses against Alternaria brassicicola in Arabidopsis

2020 ◽  
Vol 21 (23) ◽  
pp. 9196
Author(s):  
Chang Ho Kang ◽  
Joung Hun Park ◽  
Eun Seon Lee ◽  
Seol Ki Paeng ◽  
Ho Byoung Chae ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Structural Modification ◽  
Quantitative Polymerase Chain Reaction ◽  
Defense Responses ◽  
Alternaria Brassicicola ◽  
Low Molecular Weight ◽  
Biological Processes ◽  
Wild Type ◽  
Molecular Sensor ◽  
Polymerase Chain

In plants, thioredoxin (TRX) family proteins participate in various biological processes by regulating the oxidative stress response. However, their role in phytohormone signaling remains largely unknown. In this study, we investigated the functions of TRX proteins in Arabidopsis thaliana. Quantitative polymerase chain reaction (qPCR) experiments revealed that the expression of ARABIDOPSIS NUCLEOREDOXIN 1 (AtNRX1) is specifically induced by the application of jasmonic acid (JA) and upon inoculation with a necrotrophic fungal pathogen, Alternaria brassicicola. The AtNRX1 protein usually exists as a low molecular weight (LMW) monomer and functions as a reductase, but under oxidative stress AtNRX1 transforms into polymeric forms. However, the AtNRX1M3 mutant protein, harboring four cysteine-to-serine substitutions in the TRX domain, did not show structural modification under oxidative stress. The Arabidopsisatnrx1 null mutant showed greater resistance to A. brassicicola than wild-type plants. In addition, plants overexpressing both AtNRX1 and AtNRX1M3 were susceptible to A. brassicicola infection. Together, these findings suggest that AtNRX1 normally suppresses the expression of defense-responsive genes, as if it were a safety pin, but functions as a molecular sensor through its redox-dependent structural modification to induce disease resistance in plants.

scholarly journals 4-PHENYLBUTYRATE: MOLECULAR MECHANISMS AND AGING INTERVENTION POTENTIAL

2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S101-S101
Author(s):  
Michael R Bene ◽  
Kevin Thyne ◽  
Jonathan Dorigatti ◽  
Adam B Salmon
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Molecular Mechanisms ◽  
Oxidative Stress Response ◽  
Chemical Chaperone ◽  
Mouse Muscle ◽  
Age Related ◽  
Primary Mouse ◽  
Wide Range

Abstract 4-Phenylbutyrate (PBA) is a FDA approved drug for treating patients with urea cycle disorders. Additionally, PBA acts upon several pathways thought of as important modifiers of aging including: histone deacetylation, proteostasis as a chemical chaperone, and stress resistance by regulating expression of oxidative stress response proteins. PBA has also been shown to extend lifespan and improve markers of age-related health in Drosophila. Due to its wide range of effects PBA has been investigated for use in numerous age-related disorders including neurodegenerative and cardiovascular diseases. To better understand the effects of PBA on the molecular level, we used both in cellulo and in vivo studies. Treatment of primary mouse fibroblasts, C2C12 mouse muscle cells, and NCTC 1469 mouse liver cells with PBA demonstrated differential responses among cell lines to upregulation of oxidative stress response and histone acetylation. Specifically, upregulation of the oxidative stress response protein DJ-1 by PBA was found to have a corresponding dose response curve to histone H3 acetylation in primary fibroblasts. To study effects of PBA in vivo, four cohorts of HET3 mice were treated with PBA at different doses in drinking water for 4 weeks. PBA was well tolerated and led to different effects on body composition dependent on the sex of mice. We are currently investigating the molecular effects of PBA treatment in multiple tissues samples from these mice. The potential of PBA to alter many fundamental pathways, and specifically those related to stress responses, make it an attractive prospect for treatment of many age-related disorders.

scholarly journals Role of Bioactive Compounds in the Regulation of Mitochondrial Dysfunctions in Brain and Age-Related Neurodegenerative Diseases

Cells ◽  
2022 ◽  
Vol 11 (2) ◽  
pp. 257
Author(s):  
Khadidja Kessas ◽  
Zhor Chouari ◽  
Imen Ghzaiel ◽  
Amira Zarrouk ◽  
Mohamed Ksila ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Bioactive Compounds ◽  
Neuronal Development ◽  
Developmental Process ◽  
Neuroprotective Effects ◽  
New Class ◽  
Disease States ◽  
Age Related ◽  
Wide Range ◽  
Neuronal Regulation

Mitochondria are multifunctional organelles that participate in a wide range of metabolic processes, including energy production and biomolecule synthesis. The morphology and distribution of intracellular mitochondria change dynamically, reflecting a cell’s metabolic activity. Oxidative stress is defined as a mismatch between the body’s ability to neutralise and eliminate reactive oxygen and nitrogen species (ROS and RNS). A determination of mitochondria failure in increasing oxidative stress, as well as its implications in neurodegenerative illnesses and apoptosis, is a significant developmental process of focus in this review. The neuroprotective effects of bioactive compounds linked to neuronal regulation, as well as related neuronal development abnormalities, will be investigated. In conclusion, the study of secondary components and the use of mitochondrial features in the analysis of various neurodevelopmental diseases has enabled the development of a new class of mitochondrial-targeted pharmaceuticals capable of alleviating neurodegenerative disease states and enabling longevity and healthy ageing for the vast majority of people.

Sign in / Sign up

Export Citation Format

Share Document