scholarly journals Evolution Shapes the Gene Expression Response to Oxidative Stress

2019 ◽  
Vol 20 (12) ◽  
pp. 3040 ◽  
Author(s):  
Rima Siauciunaite ◽  
Nicholas S. Foulkes ◽  
Viola Calabrò ◽  
Daniela Vallone
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Molecular Mechanisms ◽  
Survival Strategies ◽  
Cell Physiology ◽  
Gene Expression Response ◽  
Low Levels ◽  
Expression Response ◽  
Species Specific ◽  
And Function

Reactive oxygen species (ROS) play a key role in cell physiology and function. ROS represents a potential source of damage for many macromolecules including DNA. It is thought that daily changes in oxidative stress levels were an important early factor driving evolution of the circadian clock which enables organisms to predict changes in ROS levels before they actually occur and thereby optimally coordinate survival strategies. It is clear that ROS, at relatively low levels, can serve as an important signaling molecule and also serves as a key regulator of gene expression. Therefore, the mechanisms that have evolved to survive or harness these effects of ROS are ancient evolutionary adaptations that are tightly interconnected with most aspects of cellular physiology. Our understanding of these mechanisms has been mainly based on studies using a relatively small group of genetic models. However, we know comparatively little about how these mechanisms are conserved or have adapted during evolution under different environmental conditions. In this review, we describe recent work that has revealed significant species-specific differences in the gene expression response to ROS by exploring diverse organisms. This evidence supports the notion that during evolution, rather than being highly conserved, there is inherent plasticity in the molecular mechanisms responding to oxidative stress.

scholarly journals Early Transcriptomic Response to OxLDL in Human Retinal Pigment Epithelial Cells

2020 ◽  
Vol 21 (22) ◽  
pp. 8818
Author(s):  
Diwa Koirala ◽  
Sarka Beranova-Giorgianni ◽  
Francesco Giorgianni
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Circadian Rhythm ◽  
Retinal Pigment ◽  
Early Gene ◽  
Low Density ◽  
Transcriptomic Response ◽  
Gene Expression Response ◽  
Gene Transcripts ◽  
Expression Response

In the sub-retinal pigment epithelium (sub-RPE) space of the aging macula, deposits of oxidized phospholipids, oxidized derivatives of cholesterol and associated oxidized low-density lipoproteins (OxLDL) are considered contributors to the onset and development of age-related macular degeneration (AMD). We investigated the gene expression response of a human-derived RPE cell line exposed for short periods of time to non-cytotoxic levels of OxLDL or LDL. In our cell model, treatment with OxLDL, but not LDL, generated an early gene expression response which affected more than 400 genes. Gene pathway analysis unveiled gene networks involved in the regulation of various cellular functions, including acute response to oxidative stress via up-regulation of antioxidative gene transcripts controlled by nuclear factor erythroid-2 related factor 2 (NRF2), and up-regulation of aryl hydrocarbon receptor-controlled detoxifying gene transcripts. In contrast, circadian rhythm-controlling genes and genes involved in lipid metabolism were strongly down-regulated. Treatment with low-density lipoprotein (LDL) did not induce the regulation of these pathways. These findings show that RPE cells are able to selectively respond to the oxidized forms of LDL via the up-regulation of gene pathways involved in molecular mechanisms that minimize cellular oxidative damage, and the down-regulation of the expression of genes that regulate the intracellular levels of lipids and lipid derivatives. The effect on genes that control the cellular circadian rhythm suggests that OxLDL might also disrupt the circadian clock-dependent phagocytic activity of the RPE. The data reveal a complex cellular response to a highly heterogeneous oxidative stress-causing agent such as OxLDL commonly present in drusen formations.

scholarly journals Cellular Response against Oxidative Stress, a Novel Insight into Lupus Nephritis Pathogenesis

2021 ◽  
Vol 11 (8) ◽  
pp. 693
Author(s):  
Corina Daniela Ene ◽  
Simona Roxana Georgescu ◽  
Mircea Tampa ◽  
Clara Matei ◽  
Cristina Iulia Mitran ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lupus Nephritis ◽  
Cellular Response ◽  
Molecular Mechanisms ◽  
Control Group ◽  
Dna Repair Mechanisms ◽  
Glycation End Products ◽  
Repair Mechanisms ◽  
Low Levels ◽  
Defective Dna Repair

The interaction of reactive oxygen species (ROS) with lipids, proteins, nucleic acids and hydrocarbonates promotes acute and chronic tissue damage, mediates immunomodulation and triggers autoimmunity in systemic lupus erythematous (SLE) patients. The aim of the study was to determine the pathophysiological mechanisms of the oxidative stress-related damage and molecular mechanisms to counteract oxidative stimuli in lupus nephritis. Our study included 38 SLE patients with lupus nephritis (LN group), 44 SLE patients without renal impairment (non-LN group) and 40 healthy volunteers as control group. In the present paper, we evaluated serum lipid peroxidation, DNA oxidation, oxidized proteins, carbohydrate oxidation, and endogenous protective systems. We detected defective DNA repair mechanisms via 8-oxoguanine-DNA-glycosylase (OGG1), the reduced regulatory effect of soluble receptor for advanced glycation end products (sRAGE) in the activation of AGE-RAGE axis, low levels of thiols, disulphide bonds formation and high nitrotyrosination in lupus nephritis. All these data help us to identify more molecular mechanisms to counteract oxidative stress in LN that could permit a more precise assessment of disease prognosis, as well as developing new therapeutic targets.

Gene expression response of mouse lung, liver and white adipose tissue to β-carotene supplementation, knockout of Bcmo1 and sex

2011 ◽  
Vol 55 (10) ◽  
pp. 1466-1474 ◽  
Author(s):  
Yvonne G. J. van Helden ◽  
Roger W. L. Godschalk ◽  
Johannes von Lintig ◽  
Georg Lietz ◽  
Jean-Francois Landrier ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Mouse Lung ◽  
Gene Expression Response ◽  
Expression Response ◽  
Β Carotene

Gene expression response of the alga Fucus virsoides (Fucales, Ochrophyta) to glyphosate solution exposure

2020 ◽  
Vol 267 ◽  
pp. 115483
Author(s):  
Marco Gerdol ◽  
Andrea Visintin ◽  
Sara Kaleb ◽  
Francesca Spazzali ◽  
Alberto Pallavicini ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Expression Response ◽  
Expression Response

scholarly journals VExD: A curated resource for human gene expression following viral infection

2021 ◽  
Author(s):  
Phillip J Dexheimer ◽  
Mario Pujato ◽  
Krishna Roskin ◽  
Matthew T Weirauch
Keyword(s):  
Gene Expression ◽  
Viral Infection ◽  
Human Gene ◽  
Application Programming Interface ◽  
Gene Expression Response ◽  
Human Gene Expression ◽  
Link Type ◽  
Uniform Manner ◽  
Expression Response ◽  
Virus Expression

AbstractMotivationHuman viruses cause significant mortality, morbidity, and economic disruption worldwide. The human gene expression response to viral infection can yield important insights into the detrimental effects to the host. To date, hundreds of studies have performed genome-scale profiling of the effect of viral infection on human gene expression. However, no resource exists that aggregates human expression results across multiple studies, viruses, and tissue types.ResultsWe developed the Virus Expression Database (VExD), a comprehensive curated resource of transcriptomic studies of viral infection in human cells. We have processed all studies within VExD in a uniform manner, allowing users to easily compare human gene expression changes across conditions.Availability and ImplementationVExD is freely accessible at https://vexd.cchmc.org for all modern web browsers. An Application Programming Interface (API) for VExD is also available. The source code is available at https://github.com/pdexheimer/[email protected], [email protected]

scholarly journals Disruption of TFIIH activities generates a stress gene expression response and reveals possible new targets against cancer

2019 ◽  
Author(s):  
Maritere Urioistegui-Arcos ◽  
Rodrigo Aguayo-Ortiz ◽  
María del Pilar Valencia-Morales ◽  
Erika Melchy-Pérez ◽  
Yvonne Rosenstein ◽  
...  
Keyword(s):  
Gene Expression ◽  
Tumour Growth ◽  
Transformed Cells ◽  
Rna Seq ◽  
Gene Expression Response ◽  
New Targets ◽  
Increased Sensitivity ◽  
Promoter Occupancy ◽  
Expression Response ◽  
Stress Gene

AbstractDisruption of the enzymatic activities of the transcription factor TFIIH by Triptolide (TPL) or THZ1 could be used against cancer. Here, we used an oncogenesis model to compare the effect of TFIIH inhibitors between transformed cells and their progenitors. We report that tumour cells exhibited highly increased sensitivity to TPL or THZ1 and that the combination of both had an additive effect. TPL affects the interaction between XPB and P52, causing a reduction in the levels of XPB, P52, and P8, but not other TFIIH subunits. RNA-Seq and RNAPII-ChIP-Seq experiments showed that although the levels of many transcripts were reduced, the levels of a significant number were increased after TPL treatment, with maintained or increased RNAPII promoter occupancy. A significant number of these genes encode for factors that have been related to tumour growth and metastasis. Some of these genes were also overexpressed in response to THZ1, which depletion enhances the toxicity of TPL and are possible new targets against cancer.

The expanding world of metabolic enzymes moonlighting as RNA binding proteins

2021 ◽  
Author(s):  
Nicole J. Curtis ◽  
Constance J. Jeffery
Keyword(s):  
Gene Expression ◽  
Regulatory Networks ◽  
Binding Proteins ◽  
Molecular Mechanisms ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Molecular Structures ◽  
Intermediary Metabolism ◽  
The Many ◽  
And Function

RNA binding proteins play key roles in many aspects of RNA metabolism and function, including splicing, transport, translation, localization, stability and degradation. Within the past few years, proteomics studies have identified dozens of enzymes in intermediary metabolism that bind to RNA. The wide occurrence and conservation of RNA binding ability across distant branches of the evolutionary tree suggest that these moonlighting enzymes are involved in connections between intermediary metabolism and gene expression that comprise far more extensive regulatory networks than previously thought. There are many outstanding questions about the molecular structures and mechanisms involved, the effects of these interactions on enzyme and RNA functions, and the factors that regulate the interactions. The effects on RNA function are likely to be wider than regulation of translation, and some enzyme–RNA interactions have been found to regulate the enzyme's catalytic activity. Several enzyme–RNA interactions have been shown to be affected by cellular factors that change under different intracellular and environmental conditions, including concentrations of substrates and cofactors. Understanding the molecular mechanisms involved in the interactions between the enzymes and RNA, the factors involved in regulation, and the effects of the enzyme–RNA interactions on both the enzyme and RNA functions will lead to a better understanding of the role of the many newly identified enzyme–RNA interactions in connecting intermediary metabolism and gene expression.

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