scholarly journals Identification of novel small RNAs in Burkholderia cenocepacia KC-01 expressed under iron limitation and oxidative stress conditions

Microbiology ◽  
2017 ◽  
Vol 163 (12) ◽  
pp. 1924-1936 ◽  
Author(s):  
Suparna Ghosh ◽  
Chetna Dureja ◽  
Indu Khatri ◽  
Srikrishna Subramanian ◽  
Saumya Raychaudhuri ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Small Rnas ◽  
Stress Conditions ◽  
Iron Limitation ◽  
Burkholderia Cenocepacia ◽  
And Oxidative Stress

A review on interplay between small RNAs and oxidative stress in cancer progression

2021 ◽  
Author(s):  
Aparimita Das ◽  
Harsha Ganesan ◽  
Sushmitha Sriramulu ◽  
Francesco Marotta ◽  
N. R. Rajesh Kanna ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cancer Progression ◽  
Small Rnas ◽  
And Oxidative Stress

scholarly journals Intra-Vitreal Administration of Microvesicles Derived from Human Adipose-Derived Multipotent Stromal Cells Improves Retinal Functionality in Dogs with Retinal Degeneration

2019 ◽  
Vol 8 (4) ◽  
pp. 510
Author(s):  
Anna Cislo-Pakuluk ◽  
Agnieszka Smieszek ◽  
Natalia Kucharczyk ◽  
Peter G.C. Bedford ◽  
Krzysztof Marycz
Keyword(s):  
Oxidative Stress ◽  
Retinal Degeneration ◽  
Stromal Cells ◽  
Clinical Studies ◽  
Stress Conditions ◽  
In Vitro Assays ◽  
Multipotent Stromal Cells ◽  
Mitochondrial Potential ◽  
And Oxidative Stress

This study was designed to determine the influence of microvesicles (MVs) derived from multipotent stromal cells isolated from human adipose tissue (hASCs) on retinal functionality in dogs with various types of retinal degeneration. The biological properties of hASC-MVs were first determined using an in vitro model of retinal Muller-like cells (CaMLCs). The in vitro assays included analysis of hASC-MVs influence on cell viability and metabolism. Brain-derived neurotrophic factor (BDNF) expression was also determined. Evaluation of the hASC-MVs was performed under normal and oxidative stress conditions. Preliminary clinical studies were performed on ten dogs with retinal degeneration. The clinical studies included behavioral tests, fundoscopy and electroretinography before and after hASC-MVs intra-vitreal injection. The in vitro study showed that CaMLCs treated with hASC-MVs were characterized by improved viability and mitochondrial potential, both under normal and oxidative stress conditions. Additionally, hASC-MVs under oxidative stress conditions reduced the number of senescence-associated markers, correlating with the increased expression of BDNF. The preliminary clinical study showed that the intra-vitreal administration of hASC-MVs significantly improved the dogs’ general behavior and tracking ability. Furthermore, fundoscopy demonstrated that the retinal blood vessels appeared to be less attenuated, and electroretinography using HMsERG demonstrated an increase in a- and b-wave amplitude after treatment. These results shed promising light on the application of cell-free therapies in veterinary medicine for retinal degenerative disorders treatment.

scholarly journals Tremella fuciformis Polysaccharides Attenuate Oxidative Stress and Inflammation in Macrophages through miR-155

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Yang Ruan ◽  
Hong Li ◽  
Lianmei Pu ◽  
Tao Shen ◽  
Zening Jin
Keyword(s):  
Oxidative Stress ◽  
Small Rnas ◽  
Nuclear Translocation ◽  
Raw264.7 Cells ◽  
Ros Production ◽  
Oxygen Species ◽  
Tremella Fuciformis ◽  
Mtt Assays ◽  
And Oxidative Stress ◽  
Inflammatory Effect

Aim. To investigate the function of Tremella fuciformis polysaccharides (TFPS) in LPS-induced inflammation and oxidative stress of macrophages. Methods. RAW264.7 cells were pretreated with TFPS and then stimulated with 0.1 μg/ml LPS. NFκB, Akt, p38MAPK, MCP-1, and SOD-1 were analyzed by Western blotting. Cell viability was measured using MTT assays. Reactive oxygen species (ROS) production, real-time PCR, ELISA, and immunofluorescence staining were performed on RAW264.7 cells that were treated with LPS and/or TFPS to investigate the anti-inflammatory effect of TFPS. Results. LPS induced inflammation and ROS production and promoted the secretion of cytokines such as TNF-α and IL-6. LPS also enhanced the nuclear translocation of NFκB, which promoted inflammation by oxidative stress. However, pretreatment with TFPS profoundly inhibited the activation of Akt, p38MAPK, and NFκB and attenuated the expression of MCP-1 in macrophages. Meanwhile, TFPS also decreased cytokine and ROS levels and attenuated cell inflammation after treatment with LPS. Moreover, miR-155, one of the key small RNAs which regulate NFκB and inflammation in macrophages, was significantly downregulated. Conclusion. TFPS inhibits LPS-induced oxidative stress and inflammation by inhibiting miR-155 expression and NFκB activation in macrophages, which suggests that TFPS may be a potential reagent for inhibiting the development of inflammation.

scholarly journals Differential Expression of sigH Paralogs during Growth and under Different Stress Conditions in Mycobacterium smegmatis

2009 ◽  
Vol 191 (8) ◽  
pp. 2888-2893 ◽  
Author(s):  
Anirudh K. Singh ◽  
Bhupendra N. Singh
Keyword(s):  
Oxidative Stress ◽  
Stationary Phase ◽  
Reverse Transcriptase ◽  
Real Time ◽  
Differential Expression ◽  
Mycobacterium Smegmatis ◽  
Stress Conditions ◽  
Pcr Analysis ◽  
Stages Of Growth ◽  
And Oxidative Stress

ABSTRACT SigH regulates a transcriptional network that responds to heat and oxidative stress in mycobacteria. Seven sigH paralogs are reported to exist in the Mycobacterium smegmatis genome. A comprehensive real-time reverse transcriptase PCR analysis during different stages of growth and upon exposure to various stress conditions and antimycobacterial compounds showed differential expression of sigH paralogs during stationary phase and severalfold increases in the levels of transcription of sigH1, sigH4, sigH5, sigH6, and sigH7 under specific stress conditions.

scholarly journals Stringent Response Governs the Virulence and Oxidative Stress Resistance of Francisella tularensis

2019 ◽  
Author(s):  
Zhuo Ma ◽  
Kayla King ◽  
Maha Alqahtani ◽  
Madeline Worden ◽  
Parthasarthy Muthuraman ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Francisella Tularensis ◽  
Stress Resistance ◽  
Stringent Response ◽  
Oxidative Stress Response ◽  
Stress Conditions ◽  
Gram Negative ◽  
And Oxidative Stress ◽  
Starvation Conditions

AbstractFrancisella tularensis is a Gram-negative bacterium responsible for causing tularemia in the northern hemisphere. F. tularensis has long been developed as a biological weapon due to its ability to cause severe illness upon inhalation of as few as ten organisms and based on its potential to be used as a bioterror agent is now classified as a Tier 1 Category A select agent by the CDC. The stringent response facilitates bacterial survival under nutritionally challenging starvation conditions. The hallmark of stringent response is the accumulation of the effector molecules ppGpp and (p)ppGpp known as stress alarmones. The relA and spoT gene products generate alarmones in several Gram-negative bacterial pathogens. RelA is a ribosome-associated ppGpp synthetase that gets activated under amino acid starvation conditions whereas, SpoT is a bifunctional enzyme with both ppGpp synthetase and ppGpp hydrolase activities. Francisella encodes a monofunctional RelA and a bifunctional SpoT enzyme. Previous studies have demonstrated that stringent response under nutritional stresses increases expression of virulence-associated genes encoded on Francisella Pathogenicity Island. This study investigated how stringent response governs the oxidative stress response of F. tularensis. We demonstrate that RelA/SpoT-mediated ppGpp production alters global gene transcriptional profile of F. tularensis in the presence of oxidative stress. The lack of stringent response in relA/spoT gene deletion mutants of F. tularensis makes bacteria more susceptible to oxidants, attenuates survival in macrophages, and virulence in mice. Mechanistically, we provide evidence that the stringent response in Francisella contributes to oxidative stress resistance by enhancing the production of antioxidant enzymes.ImportanceThe unique intracellular life cycle of Francisella in addition to nutritional stress also exposes the bacteria to oxidative stress conditions upon its brief residence in the phagosomes, and escape into the cytosol where replication takes place. However, the contribution of the stringent response in gene regulation and management of the oxidative stress response when Francisella is experiencing oxidative stress conditions is not known. Our results provide a link between the stringent and oxidative stress responses. This study further improves our understanding of the intracellular survival mechanisms of F. tularensis.

scholarly journals Low iron-induced small RNA BrrF regulates central metabolism and oxidative stress responses in Burkholderia cenocepacia

2019 ◽  
Author(s):  
Andrea Sass ◽  
Tom Coenye
Keyword(s):  
Oxidative Stress ◽  
Small Rna ◽  
Deletion Mutant ◽  
Wild Type Strain ◽  
Tca Cycle ◽  
Burkholderia Cenocepacia ◽  
Iron Starvation ◽  
Iron Depletion ◽  
In The Wild ◽  
And Oxidative Stress

AbstractBrrF is a Fur-regulated small RNA highly upregulated in Burkholderia cenocepacia under conditions of iron depletion. Its computationally predicted targets include iron-containing enzymes of the tricarboxylic acid (TCA) cycle such as aconitase and succinate dehydrogenase, as well as iron-containing enzymes responsible for the oxidative stress response, such as superoxide dismutase and catalase. Phenotypic and gene expression analysis of BrrF deletion and overexpression mutants show that the regulation of these genes is BrrF-dependent. Expression of acnA, fumA, sdhA and sdhC was downregulated during iron depletion in the wild type strain, but not in a BrrF deletion mutant. TCA cycle genes not predicted as target for BrrF were not affected in the same manner by iron depletion. Likewise, expression of sodB and katB was dowregulated during iron depletion in the wild type strain, but not in a BrrF deletion mutant. BrrF overexpression reduced aconitase and superoxide dismutase activities and increased sensitivity to hydrogen peroxide. All phenotypes and gene expression changes of the BrrF deletion mutant could be complemented by overexpressing BrrF in trans. Overall, BrrF acts as a regulator of central metabolism and oxidative stress response, possibly as an iron-sparing measure to maintain iron homeostasis under conditions of iron starvation.ImportanceRegulatory small RNAs play an essential role in maintaining cell homeostasis in bacteria in response to environmental stresses such as iron starvation. Prokaryotes generally encode a large number of RNA regulators, yet their identification and characterisation is still in its infancy for most bacterial species. Burkholderia cenocepacia is an opportunistic pathogen with high innate antimicrobial resistance, which can cause the often fatal cepacia syndrome in individuals with cystic fibrosis. In this study we characterise a small RNA which is involved in the response to iron starvation, a condition that pathogenic bacteria are likely to encounter in the host.

scholarly journals Oxidative stress induces cell death partially by decreasing both mRNA and protein levels of nicotinamide phosphoribosyltransferase in differentiated PC12 cells

PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e11401
Author(s):  
Cuiyan Zhou ◽  
Weihai Ying
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Cell Survival ◽  
Pc12 Cells ◽  
Neurological Diseases ◽  
Biological Effects ◽  
Stress Conditions ◽  
Nicotinamide Phosphoribosyltransferase ◽  
Differentiated Pc12 Cells ◽  
And Oxidative Stress

Background. Multiple studies have indicated crucial roles of NAD+ deficiency in several neurological diseases and aging. It is critical to discover the mechanisms underlying the NAD+ deficiency. A decreased level of Nicotinamide phosphoribosyltransferase (Nampt)—an important enzyme in the salvage pathway of NAD+ synthesis—has been found under certain pathological conditions, while the mechanisms underlying the Nampt decrease are unclear. The purpose of this study is to test the hypothesis that oxidative stress can produce decreased Nampt, and to investigate the biological effects of Nampt on NAD+ synthesis and cell survival under both basal and oxidative stress conditions. Methods. We used differentiated PC12 cells as a cellular model to investigate the effects of oxidative stress on the levels of Nampt. Multiple assays, including flow cytometry-based cell death assays and NAD+ assays were conducted. Results. First, oxidative stress can decrease the levels of Nampt mRNA and Nampt protein; second, Nampt plays significant roles in NAD+ synthesis under both basal conditions and oxidative stress conditions; third, Nampt plays critical roles in cell survival under both basal conditions and oxidative stress conditions; and fourth, oxidative stress produced decreased NAD+ levels and cell survival partially by decreasing Nampt. Collectively, our study has indicated that oxidative stress is a pathological factor leading to decreased Nampt, which plays important roles in oxidative stress-produced decreases in NAD+ levels and cell survival. Our findings have indicated major roles of Nampt in maintaining NAD+ levels and cell survival under both basal and oxidative stress conditions.

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