scholarly journals Stress-induced Differential Gene Expression in Cardiac Tissue

2021 ◽  
Author(s):  
Ana Elisa de Carvalho ◽  
Marco Cordeiro ◽  
Luana Rodrigues ◽  
Daniela Ortolani ◽  
Regina Spadari
Keyword(s):  
Gene Expression ◽  
Stress Response ◽  
Left Ventricle ◽  
Cardiac Tissue ◽  
Heart Function ◽  
Stressful Situation ◽  
Number Of Genes ◽  
Differential Gene ◽  
Adaptive Reaction ◽  
Shock Stress

Abstract The stress response is adaptive and aims to guarantee survival. However, the persistence of a stressor can culminate in pathology. Catecholamines released as part of the stress response over activate beta adrenoceptors (β-AR) in the heart. Whether and how stress affects the expression of components of the intracellular environment in the heart is still, however, unknown. This paper used microarray to analyze the gene expression in the left ventricle wall of rats submitted to foot shock stress, treated or not treated with the selective β2-AR antagonist ICI118,551 (ICI), compared to those of non-stressed rats also treated or not with ICI, respectively. The main findings were that stress induces changes in gene expression in the heart and that β2-AR plays a role in this process. The vast majority of genes disregulated by stress were exclusive for only one of the comparisons, indicating that, in the same stressful situation, the profile of gene expression in the heart is substantially different when the β2-AR is active or when it is blocked. Stress induced alterations in the expression of such a large number of genes seems to be an adaptive reaction, aimed at sustaining heart function and protecting cardiomyocytes from apoptosis.

scholarly journals Stress-induced differential gene expression in cardiac tissue

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ana Elisa T. S. de Carvalho ◽  
Marco A. Cordeiro ◽  
Luana S. Rodrigues ◽  
Daniela Ortolani ◽  
Regina C. Spadari
Keyword(s):  
Gene Expression ◽  
Stress Response ◽  
Left Ventricle ◽  
Differential Gene Expression ◽  
Cardiac Tissue ◽  
Stressful Situation ◽  
Adaptive Mechanism ◽  
Number Of Genes ◽  
Differential Gene ◽  
Shock Stress

AbstractThe stress response is adaptive and aims to guarantee survival. However, the persistence of a stressor can culminate in pathology. Catecholamines released as part of the stress response over activate beta adrenoceptors (β-AR) in the heart. Whether and how stress affects the expression of components of the intracellular environment in the heart is still, however, unknown. This paper used microarray to analyze the gene expression in the left ventricle wall of rats submitted to foot shock stress, treated or not treated with the selective β2-AR antagonist ICI118,551 (ICI), compared to those of non-stressed rats also treated or not with ICI, respectively. The main findings were that stress induces changes in gene expression in the heart and that β2-AR plays a role in this process. The vast majority of genes disregulated by stress were exclusive for only one of the comparisons, indicating that, in the same stressful situation, the profile of gene expression in the heart is substantially different when the β2-AR is active or when it is blocked. Stress induced alterations in the expression of such a large number of genes seems to be part of stress-induced adaptive mechanism.

scholarly journals ABSENCE OF OXIDATIVE STRESS AND SIRTUINS RECRUITMENT ON CARDIAC TISSUE POST STRESS

2022 ◽  
pp. 19
Author(s):  
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Cardiac Tissue ◽  
Heart Function ◽  
Sympathetic Nerves ◽  
Cellular Stress Response ◽  
Nadh Ratio ◽  
Pharmacological Blockade ◽  
Post Stress ◽  
Shock Stress

Stress has emerged as a factor associated with cardiovascular disease. Catecholamines released during the stress reaction by the sympathetic nerves and the adrenal medulla couple to β1-and β2-adrenoceptors in the cardiomyocytes membrane enhancing heart function in order to attend the organism demand. This might produce excessive reactive oxygen species what may culminate with oxidative stress and progression of several cardiac diseases. Sirtuins have been described as cardioprotective factors and important regulators of the cellular stress response in the heart. The aim of this work is to investigate the putative participation of oxidative stress and sirtuins in the heart of rats submitted to foot shock stress, an experimental model where there is up regulation of β2-adrenoceptors and downregulation of β1-adrenoceptors. The data have shown that in the myocardium of rats submitted to foot shock stress the H2O2 concentration, catalase and superoxide dismutase activity, NAD+/NADH ratio, as well as the protein expression of sirtuins 1 and 3 were not altered. Pharmacological blockade of the β2-adrenoceptors by ICI118,551, did not modify this scenario. It is concluded that foot shock stress does not cause disruptions in oxidative stress or redox state processes in the myocardium, and consequently, sirtuins are not recruited to stress response.

scholarly journals Differential Gene Expression Reveals Candidate Genes for Drought Stress Response in Abies alba (Pinaceae)

PLoS ONE ◽  
2015 ◽  
Vol 10 (4) ◽  
pp. e0124564 ◽  
Author(s):  
David Behringer ◽  
Heike Zimmermann ◽  
Birgit Ziegenhagen ◽  
Sascha Liepelt
Keyword(s):  
Gene Expression ◽  
Drought Stress ◽  
Stress Response ◽  
Candidate Genes ◽  
Differential Gene Expression ◽  
Abies Alba ◽  
Differential Gene

scholarly journals Direct link between metabolic regulation and the heat-shock response through the transcriptional regulator PGC-1α

2015 ◽  
Vol 112 (42) ◽  
pp. E5669-E5678 ◽  
Author(s):  
Neri Minsky ◽  
Robert G. Roeder
Keyword(s):  
Gene Expression ◽  
Stress Response ◽  
Heat Shock ◽  
Metabolic Regulation ◽  
Hormone Receptors ◽  
Transcriptional Networks ◽  
Direct Link ◽  
Heat Shock Stress ◽  
Metabolic Genes ◽  
Shock Stress

In recent years an extensive effort has been made to elucidate the molecular pathways involved in metabolic signaling in health and disease. Here we show, surprisingly, that metabolic regulation and the heat-shock/stress response are directly linked. Peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), a critical transcriptional coactivator of metabolic genes, acts as a direct transcriptional repressor of heat-shock factor 1 (HSF1), a key regulator of the heat-shock/stress response. Our findings reveal that heat-shock protein (HSP) gene expression is suppressed during fasting in mouse liver and in primary hepatocytes dependent on PGC-1α. HSF1 and PGC-1α associate physically and are colocalized on several HSP promoters. These observations are extended to several cancer cell lines in which PGC-1α is shown to repress the ability of HSF1 to activate gene-expression programs necessary for cancer survival. Our study reveals a surprising direct link between two major cellular transcriptional networks, highlighting a previously unrecognized facet of the activity of the central metabolic regulator PGC-1α beyond its well-established ability to boost metabolic genes via its interactions with nuclear hormone receptors and nuclear respiratory factors. Our data point to PGC-1α as a critical repressor of HSF1-mediated transcriptional programs, a finding with possible implications both for our understanding of the full scope of metabolically regulated target genes in vivo and, conceivably, for therapeutics.

Allele-Specific Expression and Evolution of Gene Regulation Underlying Acute Heat Stress Response and Local Adaptation in the Copepod Tigriopus californicus

2020 ◽  
Vol 111 (6) ◽  
pp. 539-547
Author(s):  
Sumaetee Tangwancharoen ◽  
Brice X Semmens ◽  
Ronald S Burton
Keyword(s):  
Gene Expression ◽  
Heat Stress ◽  
Stress Response ◽  
Local Adaptation ◽  
F1 Hybrids ◽  
Specific Expression ◽  
Heat Stress Response ◽  
Acute Heat Stress ◽  
Number Of Genes ◽  
Allele Specific

Abstract Geographic variation in environmental temperature can select for local adaptation among conspecific populations. Divergence in gene expression across the transcriptome is a key mechanism for evolution of local thermal adaptation in many systems, yet the genetic mechanisms underlying this regulatory evolution remain poorly understood. Here we examine gene expression in 2 locally adapted Tigriopus californicus populations (heat tolerant San Diego, SD, and less tolerant Santa Cruz, SC) and their F1 hybrids during acute heat stress response. Allele-specific expression (ASE) in F1 hybrids was used to determine cis-regulatory divergence. We found that the number of genes showing significant allelic imbalance increased under heat stress compared to unstressed controls. This suggests that there is significant population divergence in cis-regulatory elements underlying heat stress response. Specifically, the number of genes showing an excess of transcripts from the more thermal tolerant (SD) population increased with heat stress while that number of genes with an SC excess was similar in both treatments. Inheritance patterns of gene expression also revealed that genes displaying SD-dominant expression phenotypes increase in number in response to heat stress; that is, across loci, gene expression in F1’s following heat stress showed more similarity to SD than SC, a pattern that was absent in the control treatment. The observed patterns of ASE and inheritance of gene expression provide insight into the complex processes underlying local adaptation and thermal stress response.

scholarly journals Stress response in tardigrades: differential gene expression of molecular chaperones

2009 ◽  
Vol 15 (4) ◽  
pp. 423-430 ◽  
Author(s):  
Andy Reuner ◽  
Steffen Hengherr ◽  
Brahim Mali ◽  
Frank Förster ◽  
Detlev Arndt ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stress Response ◽  
Differential Gene Expression ◽  
Molecular Chaperones ◽  
Differential Gene

scholarly journals Gene expression profiling of Tea (Camellia sinensis L.) in response to biotic stress using microarrays

2020 ◽  
Author(s):  
S. Ashokraj ◽  
E. Edwin Raj ◽  
K.N. Chandrashekara ◽  
R. Govindaraj ◽  
T. Femlin Blessia ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stress Response ◽  
Differential Gene Expression ◽  
Microarray Analysis ◽  
Biotic Stress ◽  
Differentially Expressed ◽  
Regulatory Function ◽  
Biotic Stress Response ◽  
Differential Gene ◽  
Tea Plants

ABSTRACTThe blister blight (BB) and grey blight (GB) diseases are the major biotic stresses, which affecting the plant health, yield and quality of tea. The study aims to understand the gene response of tea plants against destructing foliar diseases in terms of differential gene expression and their pathways through microarray analysis aid by MapMan® software. The results of expression profile analysis showed that 235 in BB and 258 for GB genes were differentially expressed (at P<0.05) which involving in gene regulatory function as biotic stress response. Similarly, 76 and 86 differentially expressed genes involving in cellular response during BB and GB diseases, respectively. However, 28 in BB and 9 in GB differentially expressed (P<0.01) genes were putatively involved in biotic stress response. The study also identified differentially expressed 75 transcription factors (TFs) belongs to 23 TFs superfamily act as either transcriptional activators or repressors. The study helps to understand the differential gene expression pattern and its cellular, molecular and biological mechanisms of tea plants of two different diseases based on microarray analysis. Further studies using biotechnological tools on the stress-responsive genes in the germplasm may enable us for development of disease resistance.

scholarly journals Analysis of differential gene expression of heart failure based on Gene Expression Omnibus database

2020 ◽  
Author(s):  
Haifeng Yan ◽  
Xianliang Wang ◽  
Yazhu Hou ◽  
Zhihua Yang ◽  
Jingyuan Mao
Keyword(s):  
Gene Expression ◽  
Heart Failure ◽  
Extracellular Matrix ◽  
Left Ventricle ◽  
Pathway Analysis ◽  
Molecular Mechanisms ◽  
Cardiac Tissue ◽  
Gene Expression Omnibus ◽  
Differentially Expressed ◽  
Receptor Interaction

Abstract Background To screen and identify key genes involved in heart failure and explore underlying molecular mechanisms. Methods The expression profile of GSE26887 was downloaded from Gene Expression Omnibus (GEO), which contained 24 samples, including 19 left ventricle cardiac tissue of heart failure and 5 controls. The differentially expressed genes (DEGs) were obtained and got further analysis by bioinformatics methods. The DEGs and volcano plot were acquired with the use of ‘lima’ package in ‘R’ software and heat map was drawn through the ‘heatmap’ package. Gene ontology (GO) and pathway analysis of DEGs were performed by means of Database for Annotation, Visualization and Integrated Discovery (DAVID) and Kyoto Encyclopedia of Genes and Genomes (KEGG) online analyses, respectively. The DEGs interaction and network map were constructed through Search Tool for the Retrieval of Interacting Genes (STRING ) database and Cystoscope(v3.6.0)software. Results The transcriptome analysis of left ventricle cardiac tissue showed that 236 genes were differentially expressed between heart failure and control, of which 124 were significantly upregulated (P < 0.01) and 101 genes downregulated (P < 0.01). GO analysis uncovered that DEGs were enriched in extracellular space, extracellular matrix, extracellular matrix organization, cell adhesion, proteinaceous extracellular matrix and heparin binding. Thus, the function of extracellular matrix is mainly affected. The KEGG pathway enrichment indicated that the DEGs were involved in eight pathways, of these pathways, ECM-receptor interaction, Drug metabolism-cytochrome P450 and Pathogenic Escherichia coli infection are dominant. Protein-protein interaction (PPI) revealed the interactions of 30 protein products encoded of DEGs. Of the 30 protein products, the critical gene, called Interleukin-6 (IL6), was identified with the use of Cystoscope software. Conclusion Extracellular matrix and IL6 play an important role in the development of heart failure. Functional annotation and pathway analysis of these main genes were identified, which provide the basis for insight into the underlying pathogenetic mechanisms and predicting therapeutic targets of heart failure.

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