scholarly journals Arabidopsis V-ATPase d2 subunit plays a role in plant responses to oxidative stress

2020 ◽  
Author(s):  
Shuang Feng ◽  
Yun Peng ◽  
Enhui Liu ◽  
Hongping Ma ◽  
Kun Qiao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Developmental Stages ◽  
Plant Responses ◽  
Rna Seq ◽  
Wild Type ◽  
Phenotypic Analysis ◽  
Non Invasive ◽  
Atpase Gene ◽  
D Subunit ◽  
And Oxidative Stress

Abstract Background: Vacuolar-type H + -ATPase (V-ATPase) is a multisubunit proton pump located on the endomembranes, which plays an important role in plant growth. The Arabidopsis V-ATPase d subunit consists of two isoforms, AtVHA-d1 and AtVHA-d2. Results: In this study, the function of the AtVHA-d2 gene was investigated. Histochemical analysis revealed that the AtVHA-d1 and AtVHA-d2 genes were generally and highly overlapping expressed in multiple tissues at different developmental stages of Arabidopsis. Subcellular localization showed that AtVHA-d2 was mainly localized to the vacuole. The AtVHA-d2 expression was significantly induced by oxidative stress. Furthermore, the phenotypic analysis showed that the atvha-d2 mutant was sensitive to oxidative stress. The non-invasive micro-test measurement demonstrated that the net H + influx in the atvha-d2 roots was weaker than that of the wild type under normal conditions. However, oxidative stress resulted in the H + efflux in atvha-d2 roots, which was significantly different from the wild type. RNA-seq combined with qPCR analysis showed that the expression of several members of the plasma membrane H + -ATPase gene ( AtAHA ) family in atvha-d2 were significant different from wild type under normal and oxidative stress. Conclusion: Overall, our results indicate that AtVHA-d2 plays a role in Arabidopsis in response to oxidative stress by affecting H + flux and AtAHA gene expression.

scholarly journals Arabidopsis V-ATPase d2 Subunit Plays a Role in Plant Responses to Oxidative Stress

Genes ◽  
2020 ◽  
Vol 11 (6) ◽  
pp. 701 ◽  
Author(s):  
Shuang Feng ◽  
Yun Peng ◽  
Enhui Liu ◽  
Hongping Ma ◽  
Kun Qiao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Developmental Stages ◽  
Plant Responses ◽  
Rna Seq ◽  
Wild Type ◽  
Histochemical Analysis ◽  
Qpcr Analysis ◽  
Atpase Gene ◽  
In The Wild ◽  
D Subunit

Vacuolar-type H+-ATPase (V-ATPase), a multisubunit proton pump located on the endomembrane, plays an important role in plant growth. The Arabidopsis thaliana V-ATPase d subunit (VHA-d) consists of two isoforms; AtVHA-d1 and AtVHA-d2. In this study, the function of AtVHA-d2 was investigated. Histochemical analysis revealed that the expression of AtVHA-d1 and AtVHA-d2 was generally highly overlapping in multiple tissues at different developmental stages of Arabidopsis. Subcellular localization revealed that AtVHA-d2 was mainly localized to the vacuole. AtVHA-d2 expression was significantly induced by oxidative stress. Analysis of phenotypic and H2O2 content showed that the atvha-d2 mutant was sensitive to oxidative stress. The noninvasive microtest monitoring demonstrated that the net H+ influx in the atvha-d2 roots was weaker than that in the wild-type under normal conditions. However, oxidative stress resulted in the H+ efflux in atvha-d2 roots, which was significantly different from that in the wild-type. RNA-seq combined with qPCR analysis showed that the expression of several members of the plasma membrane H+-ATPase gene (AtAHA) family in atvha-d2 was significantly different from that in the wild-type. Overall, our results indicate that AtVHA-d2 plays a role in Arabidopsis in response to oxidative stress by affecting H+ flux and AtAHA gene expression.

16. Physiological effects of IDH1 loss-of-function on Chondrocyte Differentiation through Hedgehog Pathway upregulation

2018 ◽  
Author(s):  
Cassie Tyson
Keyword(s):  
Developmental Stages ◽  
Hedgehog Pathway ◽  
Chondrocyte Differentiation ◽  
Loss Of Function ◽  
Wild Type ◽  
Phenotypic Analysis ◽  
Growth Plate Chondrocytes ◽  
Idh Mutations ◽  
Cartilage Tumors ◽  
Deficient Mice

Cartilage tumors are the most common and terminal primary neoplasms in bone. Physiologically, bones formed through endochondral ossification are regulated by the Hedgehog pathway and Parathyroid hormone-like hormone feedback loop. The upregulation of the infamous Hedgehog pathway has been demonstrated in several non-cartilaginous neoplasms. Recently, frequent mutational events of isocitrate dehydrogenase1 (IDH1) were identified in cartilage tumors. In other neoplasms, IDH mutations produces an oncometabolite that can promote HIF1a activation, contributing to tumorigenesis. Currently, the role of IDH1 mutations in cartilage tumors remain unknown. Investigating the physiological aspect of IDH1proves useful in identifying novel therapeutic targets for cartilage tumors. IDH1 deficient and wild-type littermates, were harvested for forelimbs and hindlimbs at various developmental stages for phenotypic analysis via hematoxylin and eosin staining. Histological analysis demonstrated IDH1 homozygous deficient mice at embryonic stages exhibited dwarfism and an elongated layer of hypertrophic chondrocytes. This was verified via immunohistochemistry Type 10 Collagen staining and Quantitative PCR (qPCR) using the chondrocyte terminal differentiation marker Col10a1. Whole skeletons of IDH1 deficient mice were subjected to skeletal double staining which demonstrated delayed mineralization of underdeveloped IDH1 deficient mice contrasted with wild-type littermates. qPCR was performed to examine the status of chondrocyte differentiation through the Hedgehog pathway in cultured primarymouse growth plate chondrocytes. Interestingly, IDH1 deficient non-neoplastic cells revealed significant upregulation of Hedgehog target molecules in IDH1 deficient chondrocytes. As a result, the loss-offunction of IDH1 was identified as a potential impairment of chondrocyte differentiation and a factor towards chondrocyte tumorgenisis.

scholarly journals RNA-Seq Expression Analysis of Chronic Asthmatic Mice with Bu-Shen-Yi-Qi Formula Treatment and Prediction of Regulated Gene Targets of Anti-Airway Remodeling

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Jie Cui ◽  
Zexi Lv ◽  
Fangzhou Teng ◽  
La Yi ◽  
Weifeng Tang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Network ◽  
Structural Changes ◽  
Airway Remodeling ◽  
Signal Pathways ◽  
Rna Seq ◽  
Critical Nodes ◽  
Differential Expression Genes ◽  
Polymerase Chain ◽  
And Oxidative Stress

Airway remodeling is one of the typical pathological characteristics of asthma, while the structural changes of the airways in asthma are complex, which impedes the development of novel asthma targeted therapy. Our previous study had shown that Bu-Shen-Yi-Qi formula (BSYQF) could ameliorate airway remodeling in chronic asthmatic mice by modulating airway inflammation and oxidative stress in the lung. In this study, we analysed the lung transcriptome of control mice and asthmatic mouse model with/without BSYQF treatment. Using RNA-sequencing (RNA-seq) analysis, we found that 264/1746 (15.1%) of transcripts showing abnormal expression in asthmatic mice were reverted back to completely or partially normal levels by BSYQF treatment. Additionally, based on previous results, we identified 21 differential expression genes (DEGs) with fold changes (FC) > (±) 2.0 related to inflammatory, oxidative stress, mitochondria, PI3K/AKT, and MAPK signal pathways which may play important roles in the mechanism of the anti-remodeling effect of BSYQF treatment. Through inputting 21 DEGs into the IPA database to construct a gene network, we inferred Adipoq, SPP1, and TNC which were located at critical nodes in the network may be key regulators of BSYQF's anti-remodeling effect. In addition, the quantitative real-time polymerase chain reaction (qRT-PCR) result for the selected four DEGs matched those of the RNA-seq analysis. Our results provide a preliminary clue to the molecular mechanism of the anti-remodeling effect of BSYQF in asthma.

scholarly journals Endogenous Hydrogen Sulfide Is an Important Factor in Maintaining Arterial Oxygen Saturation

2021 ◽  
Vol 12 ◽  
Author(s):  
Yan Huang ◽  
Gang Wang ◽  
Zhan Zhou ◽  
Zhengshan Tang ◽  
Ningning Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Injury ◽  
Arterial Oxygen Saturation ◽  
Arterial Oxygen ◽  
Wall Thickening ◽  
Alveolar Wall ◽  
Leukocyte Infiltration ◽  
Wild Type ◽  
Interstitial Edema ◽  
And Oxidative Stress

The gasotransmitter H2S is involved in various physiological and pathophysiological processes. The aim of this study was to investigate the physiological functions of H2S in the lungs. In the model of mouse with genetic deficiency in a H2S natural synthesis enzyme cystathionine-γ-lyase (CSE), we found that arterial oxygen saturation (SaO2) was decreased compared with wild type mice. Hypoxyprobe test showed that mild hypoxia occurred in the tissues of heart, lungs and kidneys in Cse-/- mice. H2S donor GYY4137 treatment increased SaO2 and ameliorated hypoxia state in cardiac and renal tissues. Further, we revealed that lung blood perfusion and airway responsiveness were not linked to reduced SaO2 level. Lung injury was found in Cse-/- mice as evidenced by alveolar wall thickening, diffuse interstitial edema and leukocyte infiltration in pulmonary tissues. IL-8, IL-1β, and TNF-α levels were markedly increased and oxidative stress levels were also significantly higher with increased levels of the pro-oxidative biomarker, MDA, decreased levels of the anti-oxidative biomarkers, T-AOC and GSH/GSSG, and reduced superoxide dismutase (SOD) activity in lung tissues of Cse-/- mice compared with those of wild type mice. GYY4137 treatment ameliorated lung injury and suppressed inflammatory state and oxidative stress in lung tissues of Cse-/- mice. A decrease in SaO2 was found in normal mice under hypoxia. These mice displayed lung injury as evidenced by alveolar wall thickening, interstitial edema and leukocyte infiltration. Increased levels of inflammatory cytokines and oxidative stress were also found in lung tissues of the mice with hypoxia insult. GYY4137 treatment increased SaO2 and ameliorated lung injury, inflammation and oxidative stress. Our data indicate that endogenous H2S is an important factor in maintaining normal SaO2 by preventing oxidative stress and inflammation in the lungs.

scholarly journals Depicting the Core Transcriptome Modulating Multiple Abiotic Stresses Responses in Sesame (Sesamum indicum L.)

2019 ◽  
Vol 20 (16) ◽  
pp. 3930 ◽  
Author(s):  
Komivi Dossa ◽  
Marie A. Mmadi ◽  
Rong Zhou ◽  
Tianyuan Zhang ◽  
Ruqi Su ◽  
...  
Keyword(s):  
Abiotic Stresses ◽  
Meta Analysis ◽  
Plant Responses ◽  
Proof Of Concept ◽  
Rna Seq ◽  
Wild Type ◽  
Salt Treatment ◽  
Hub Genes ◽  
Hub Gene ◽  
The Core

Sesame is a source of a healthy vegetable oil, attracting a growing interest worldwide. Abiotic stresses have devastating effects on sesame yield; hence, studies have been performed to understand sesame molecular responses to abiotic stresses, but the core abiotic stress-responsive genes (CARG) that the plant reuses in response to an array of environmental stresses are unknown. We performed a meta-analysis of 72 RNA-Seq datasets from drought, waterlogging, salt and osmotic stresses and identified 543 genes constantly and differentially expressed in response to all stresses, representing the sesame CARG. Weighted gene co-expression network analysis of the CARG revealed three functional modules controlled by key transcription factors. Except for salt stress, the modules were positively correlated with the abiotic stresses. Network topology of the modules showed several hub genes predicted to play prominent functions. As proof of concept, we generated over-expressing Arabidopsis lines with hub and non-hub genes. Transgenic plants performed better under drought, waterlogging, and osmotic stresses than the wild-type plants but did not tolerate the salt treatment. As expected, the hub gene was significantly more potent than the non-hub gene. Overall, we discovered several novel candidate genes, which will fuel investigations on plant responses to multiple abiotic stresses.

Comparison of genotoxicity and oxidative stress in patients undergoing non-invasive surgery under isoflurane and propofol anaesthesia

2011 ◽  
Vol 28 ◽  
pp. 137
Author(s):  
M. G. Braz ◽  
D. T. Pierine ◽  
C. R. Correa ◽  
A. L.A. Ferreira ◽  
J. R.C. Braz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Invasive Surgery ◽  
Non Invasive ◽  
And Oxidative Stress

scholarly journals Cardiac inflammation associated with a Western diet is mediated via activation of RAGE by AGEs

2008 ◽  
Vol 295 (2) ◽  
pp. E323-E330 ◽  
Author(s):  
Christos Tikellis ◽  
Merlin C. Thomas ◽  
Brooke E. Harcourt ◽  
Melinda T. Coughlan ◽  
Josepha Pete ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Hypertrophy ◽  
Fast Food ◽  
Cardiac Injury ◽  
Western Diet ◽  
Cardiomyocyte Hypertrophy ◽  
Standard Diet ◽  
Wild Type ◽  
Cardiac Inflammation ◽  
And Oxidative Stress

A diet high in fat induces cardiac hypertrophy, inflammation, and oxidative stress. Although such actions have largely been ascribed to fat deposition, the accumulation of advanced glycation end products (AGEs) and subsequent activation of the receptor for AGEs (RAGE) may also represent important mediators of cardiac injury following exposure to a Western diet. In this study, male C57BL6J and RAGE knockout mice were placed on either a standard diet (7% fat) or a Western “fast-food” diet (21% fat). Animals receiving a high-fat diet were further randomized to receive the AGE inhibitor alagebrium chloride (1 mg·kg−1·day−1) and followed for 16 wk. A Western diet was associated with cardiac hypertrophy, inflammation, mitochondrial-dependent superoxide production, and cardiac AGE accumulation in wild-type mice. Although RAGE-KO mice fed a Western diet also became obese and accumulated intramyocardial lipid, cardiomyocyte hypertrophy, inflammation, and oxidative stress were attenuated compared with wild-type mice. Similarly, mice of both strains receiving alagebrium chloride had reduced levels of inflammation and oxidative stress, in association with a reduction in cardiac AGEs and RAGE. This study suggests that AGEs represent important mediators of cardiac injury associated with a Western fast-food diet. These data point to the potential utility of AGE-reducing strategies in the prevention and management of cardiac disease.

scholarly journals Keratin-Based Epidermal Green Autofluorescence is a Common Biomarker of Organ Injury

2019 ◽  
Author(s):  
Mingchao Zhang ◽  
Yujia Li ◽  
Jiucun Wang ◽  
Huiru Tang ◽  
Zhong Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Ischemic Stroke ◽  
Recovery Phase ◽  
The Body ◽  
Organ Injury ◽  
Lung Cancer Patients ◽  
Non Invasive ◽  
And Oxidative Stress ◽  
Invasive Evaluation

AbstractIt is critical to discover biomarkers for non-invasive evaluation of the levels of inflammation and oxidative stress in human body - two key pathological factors in numerous diseases. Our study has indicated keratin 1-based epidermal autofluorescence (AF) as a biomarker of this type: Inducers of both inflammation and oxidative stress dose-dependently increased epidermal green AF with polyhedral structure in mice, with the AF intensity being highly associated with the dosages of the inducers. Lung cancer also induced increased epidermal green AF of mice, which was mediated by inflammation. Significant and asymmetrical increases in green AF intensity with polyhedral structure were found in the Dorsal Index Fingers’ skin of acute ischemic stroke (AIS) patients. While the AF intensity of the subjects with high risk for developing AIS, ischemic stroke patients in recovery phase and lung cancer patients was significantly higher than that of healthy controls, both AF intensity and AF asymmetry of these four groups were markedly lower than those of the AIS patients, which have shown promise for AIS diagnosis. Several lines of evidence have indicated K1 as an origin of the AF, e.g., K1 siRNA administration attenuated the oxidative stress-induced AF increase of mice. Collectively, our study has indicated K1-based epidermal AF as a biomarker for non-invasive evaluation of the levels of inflammation and oxidative stress in the body. These findings have established a basis for novel keratin’s AF-based biomedical imaging technology for non-invasive, efficient and economic diagnosis and screening of such inflammation- and oxidative stress-associated diseases as AIS.

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