Cortisol signaling and stress-induced gene expressions in response to copper toxicity through heat stress during zebrafish embryogenesis

2021 ◽  
Author(s):  
Kiyun Park ◽  
Ihn-Sil Kwak
Keyword(s):  
Cell Death ◽  
Heat Stress ◽  
High Temperature ◽  
Copper Toxicity ◽  
B Cell Lymphoma ◽  
Immune Defense ◽  
Gene Expressions ◽  
Transcriptional Responses ◽  
Stress Related Genes ◽  
Zebrafish Embryogenesis

Abstract Climate change is leading to an increase in temperatures, which has a stressful impact on the aquatic environment. Cortisol signaling is involved in enhancing metabolic processes such as anti-oxidation, immune defense, and osmoregulation, under stress conditions in fish. The present study aimed at evaluating the effects of copper (Cu) toxicity along with an increase in temperature during zebrafish embryogenesis, based on the transcriptional responses of cortisol and stress-related genes. A decreased survival rate was observed following combined exposure to high temperature and Cu. Heart rates of zebrafish embryos significantly increased only during heat stress. An abnormal morphology was induced by exposure to a combination of Cu and heat stress. Furthermore, heat stress also triggered Cu-induced intracellular reactive oxygen species production with upregulation of superoxide dismutase (SOD) and glutathione s-transferase (GST) and cell death with modified expressions of p53 and B-cell lymphoma-2 (Bcl-2) in the zebrafish embryo. Finally, increased cortisol level and altered expressions of cortisol-signaling genes were observed following exposure to Cu and high temperature. These results highlight that the realistic exposure to combined stressors disturbs cortisol-related defense pathways as well as the stress-induced processes of anti-oxidation and cell death in fish.

scholarly journals Heat Treatment at an Early Age Has Effects on the Resistance to Chronic Heat Stress on Broilers

Animals ◽  
2019 ◽  
Vol 9 (12) ◽  
pp. 1022 ◽  
Author(s):  
Darae Kang ◽  
JinRyong Park ◽  
KwanSeob Shim
Keyword(s):  
Heat Stress ◽  
High Temperature ◽  
Heat Shock ◽  
Stress Hormones ◽  
Heat Exposure ◽  
Control Group ◽  
Heat Shock Factors ◽  
Gene Expressions ◽  
Stressed Group ◽  
Shock Proteins

This study was conducted to investigate the effects of early heat conditioning on growth performance, liver-specific enzymes (GOT and GPT), neuro-hormones (dopamine and serotonin), stress hormones (corticosterone), and the expression of HSPs (heat shock proteins), HSFs (heat shock factors), and pro-inflammatory cytokines under chronic high temperature. Broilers were raised with commercial feed and supplied with water ad libitum under conventional temperature. We separated the broilers into three groups: the control without any heat exposure (C), chronic heat-stressed group (CH), and early and chronic heat-stressed group (HH). At 5 days of age, the HH group was exposed to high temperatures (40 °C for 24 h), while the remaining groups were raised at a standard temperature. Between days 6 and 20, all three groups were kept under optimal temperature. From 21 to 35 days, the two heat-stressed groups (CH and HH) were exposed to 35 °C. Groups exposed to high temperature (CH and HH) showed significantly lower body weight and feed intake compared to the control. GOT and GPT were lower expressed in the CH and HH groups than the control group. In addition, the protein expressions of HSPs were down-regulated by chronic heat stress (CH and HH groups). The gene expressions of HSP60 and HSF3 were significantly down-regulated in the CH and HH groups, while HSP70 and HSP27 genes were up-regulated only in the HH group compared with the control group. The expression of pro-inflammatory cytokine genes was significantly up-regulated in the HH group compared with the control and CH groups. Thus, exposure of early Heat stress (HS) to broilers may affect the inflammatory response; however, early heat exposure did not have a positive effect on chronic HS of liver enzymes and heat shock protein expression.

High Altitude hypoxia

2020 ◽  
Vol 17 ◽  
Author(s):  
Asma Babar ◽  
Kifayatullah Mengal ◽  
Abdul Hanan Babar ◽  
Shixin Wu ◽  
Mujahid Ali Shah ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
High Altitude ◽  
Molecular Mechanisms ◽  
Strong Association ◽  
Haemoglobin Concentration ◽  
Metabolic Reprogramming ◽  
Molecular Networks ◽  
Whole Genome ◽  
Gene Expressions ◽  
Transcriptional Responses

: The world highest and largest altitude area is called the Qinghai-Tibetan plateau (QTB), which harbors unique animal and plant species. Mammals that inhabit the higher altitude regions have adapted well to the hypoxic conditions. One of the main stressors at high altitude is hypoxia. Metabolic responses to hypoxia play important roles in cell survival strategies and some diseases. However, the homeostatic alterations that equilibrate variations in the demand and supply of energy to maintain organismal function in a prolonged low O2 environment persist partly understood, making it problematic to differentiate adaptive from maladaptive responses in hypoxia. Tibetans and yaks are two perfect examples innate to the plateau for high altitude adaptation. By the scan of the whole-genome, EPAS1 and EGLN1 were identified as key genes associated with sustained haemoglobin concentration in high altitude mammals for adaptation. The yak is a much more ancient mammal which has existed on QTB longer than humans, it is, therefore, possible that natural selection represented a diverse group of genes/pathways in yaks. Physiological characteristics are extremely informative in revealing molecular networks associated with inherited adaptation, in addition to the whole-genome adaptive changes at the DNA sequence level. Gene-expression can be changed by a variety of signals originating from the environment, and hypoxia is the main factor amongst them. The hypoxia-inducible factors (HIF-1α and EPAS1/HIF-2α) are the main regulators of oxygen in homeostasis which play a role as maestro regulators of adaptation in hypoxic reaction of molecular mechanisms. (Vague) The basis of this review is to present recent information regarding the molecular mechanism involved in hypoxia that regulates candidate genes and proteins. Many transcriptional responses toward hypoxia are facilitated by HIFs that change the number of gene expressions and help in angiogenesis, erythropoiesis, metabolic reprogramming and metastasis. HIFs also activate several signals highlighting a strong association between hypoxia, the misfolded proteins’ accumulation in the endoplasmic reticulum in stress and activation of unfolded protein response (UPR). It was observed that at high-altitude, pregnancies yield a low birth weight ∼100 g per1000 m of the climb. (Vague) It may involve variation in the events of energy-demanding, like protein synthesis. Prolonged hypobaric hypoxia causes placental ER stress, which in turn, moderates protein synthesis and reduces proliferation. Further, Cardiac hypertrophy by cytosolic Ca2+ raises and Ca2+/calmodulin, calcineurin stimulation, NF-AT3 pathway might be caused by an imbalance in Sarcoplasmic reticulum ER Ca2, might be adaptive in beginning but severe later.

scholarly journals GERMINATION AND VIGOUR IN SEEDS OF THE COWPEA IN RESPONSE TO SALT AND HEAT STRESS

2019 ◽  
Vol 32 (1) ◽  
pp. 143-151 ◽  
Author(s):  
Luma Rayane de Lima Nunes ◽  
Paloma Rayane Pinheiro ◽  
Charles Lobo Pinheiro ◽  
Kelly Andressa Peres Lima ◽  
Alek Sandro Dutra
Keyword(s):  
Salt Stress ◽  
Heat Stress ◽  
High Temperature ◽  
Low Temperature ◽  
Vigna Unguiculata ◽  
Salt Concentration ◽  
Dry Weight ◽  
Germination Percentage ◽  
Different Types ◽  
Different Temperatures

ABSTRACT Salinity is prejudicial to plant development, causing different types of damage to species, or even between genotypes of the same species, with the effects being aggravated when combined with other types of stress, such as heat stress. The aim of this study was to evaluate the tolerance of cowpea genotypes (Vigna unguiculata L. Walp.) to salt stress at different temperatures. Seeds of the Pujante, Epace 10 and Marataoã genotypes were placed on paper rolls (Germitest®) moistened with different salt concentrations of 0.0 (control), 1.5, 3.0, 4.5 and 6.0 dS m-1, and placed in a germination chamber (BOD) at temperatures of 20, 25, 30 and 35°C. The experiment was conducted in a completely randomised design, in a 3 × 4 × 5 scheme of subdivided plots, with four replications per treatment. The variables under analysis were germination percentage, first germination count, shoot and root length, and total seedling dry weight. At temperatures of 30 and 35°C, increases in the salt concentration were more damaging to germination in the Epace 10 and Pujante genotypes, while for the Marataoã genotype, damage occurred at the temperature of 20°C. At 25°C, germination and vigour in the genotypes were higher, with the Pujante genotype proving to be more tolerant to salt stress, whereas Epace 10 and Marataoã were more tolerant to high temperatures. Germination in the cowpea genotypes was more sensitive to salt stress when subjected to heat stress caused by the low temperature of 20°C or high temperature of 35°C.

scholarly journals Wheat (Triticum aestivum L.) TaHMW1D Transcript Variants Are Highly Expressed in Response to Heat Stress and in Grains Located in Distal Part of the Spike

Plants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 687
Author(s):  
Chan Seop Ko ◽  
Jin-Baek Kim ◽  
Min Jeong Hong ◽  
Yong Weon Seo
Keyword(s):  
Heat Stress ◽  
High Temperature ◽  
Temperature Stress ◽  
Storage Proteins ◽  
Seed Storage ◽  
Seed Storage Proteins ◽  
Grain Filling ◽  
High Temperature Stress ◽  
Two Dimensional Gel Electrophoresis ◽  
Transcript Variants

High-temperature stress during the grain filling stage has a deleterious effect on grain yield and end-use quality. Plants undergo various transcriptional events of protein complexity as defensive responses to various stressors. The “Keumgang” wheat cultivar was subjected to high-temperature stress for 6 and 10 days beginning 9 days after anthesis, then two-dimensional gel electrophoresis (2DE) and peptide analyses were performed. Spots showing decreased contents in stressed plants were shown to have strong similarities with a high-molecular glutenin gene, TraesCS1D02G317301 (TaHMW1D). QRT-PCR results confirmed that TaHMW1D was expressed in its full form and in the form of four different transcript variants. These events always occurred between repetitive regions at specific deletion sites (5′-CAA (Glutamine) GG/TG (Glycine) or (Valine)-3′, 5′-GGG (Glycine) CAA (Glutamine) -3′) in an exonic region. Heat stress led to a significant increase in the expression of the transcript variants. This was most evident in the distal parts of the spike. Considering the importance of high-molecular weight glutenin subunits of seed storage proteins, stressed plants might choose shorter polypeptides while retaining glutenin function, thus maintaining the expression of glutenin motifs and conserved sites.

scholarly journals Progress in understanding the role of lncRNA in programmed cell death

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Na Jiang ◽  
Xiaoyu Zhang ◽  
Xuejun Gu ◽  
Xiaozhuang Li ◽  
Lei Shang
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Molecular Mechanisms ◽  
Membrane Receptors ◽  
Gene Expressions ◽  
Apoptosis Pathway ◽  
Stem Cell Pluripotency ◽  
Extrinsic Apoptosis ◽  
Related Proteins ◽  
Cycle Regulation

AbstractLong non-coding RNAs (lncRNAs) are transcripts longer than 200 nucleotides but not translated into proteins. LncRNAs regulate gene expressions at multiple levels, such as chromatin, transcription, and post-transcription. Further, lncRNAs participate in various biological processes such as cell differentiation, cell cycle regulation, and maintenance of stem cell pluripotency. We have previously reported that lncRNAs are closely related to programmed cell death (PCD), which includes apoptosis, autophagy, necroptosis, and ferroptosis. Overexpression of lncRNA can suppress the extrinsic apoptosis pathway by downregulating of membrane receptors and protect tumor cells by inhibiting the expression of necroptosis-related proteins. Some lncRNAs can also act as competitive endogenous RNA to prevent oxidation, thereby inhibiting ferroptosis, while some are known to activate autophagy. The relationship between lncRNA and PCD has promising implications in clinical research, and reports have highlighted this relationship in various cancers such as non-small cell lung cancer and gastric cancer. This review systematically summarizes the advances in the understanding of the molecular mechanisms through which lncRNAs impact PCD.

scholarly journals Predicting Responses to Checkpoint Inhibitors in Lymphoma: Are We Up to the Standards of Solid Tumors?

2020 ◽  
Vol 14 ◽  
pp. 117955492097636
Author(s):  
Ah-Reum Jeong ◽  
Edward D Ball ◽  
Aaron Michael Goodman
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
B Cell ◽  
Solid Tumors ◽  
Cell Lymphoma ◽  
Checkpoint Inhibitors ◽  
B Cell Lymphoma ◽  
Hematologic Malignancies ◽  
Checkpoint Blockade ◽  
Programmed Cell Death 1

Treatment of cancer has transformed with the introduction of checkpoint inhibitors. However, the majority of solid tumor patients do not respond to checkpoint blockade. In contrast, the response rate to programmed cell death 1 (PD-1) blockade in relapsed/refractory classical Hodgkin lymphoma (cHL) is 65% to 84% which is the highest among all cancers. Currently, checkpoint inhibitors are only approved for cHL and primary mediastinal B-cell lymphoma as the responses to single-agent checkpoint blockade in other hematologic malignancies is disappointingly low. Various established biomarkers such as programmed cell death 1 ligand 1 (PD-L1) protein surface expression, mismatch repair (MMR) status, and tumor mutational burden (TMB) are routinely used in clinical decision-making in solid tumors. In this review, we will explore these biomarkers in the context of hematologic malignancies. We review characteristic 9p24.1 structural alteration in cHL and primary mediastinal B-cell lymphoma (PMBCL) as a basis for response to PD-1 inhibition, as well as the role of antigen presentation pathways. We also explore the reported frequencies of MMR deficiency in various hematologic malignancies and investigate TMB as a predictive marker.

scholarly journals Fibrillar α-synuclein induces neurotoxic astrocyte activation via RIP kinase signaling and NF-κB

2021 ◽  
Vol 12 (8) ◽  
Author(s):  
Tsui-Wen Chou ◽  
Nydia P. Chang ◽  
Medha Krishnagiri ◽  
Aisha P. Patel ◽  
Marissa Lindman ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Biology ◽  
Molecular Mechanisms ◽  
Neurodegenerative Disorder ◽  
Neuronal Cell ◽  
Dopamine Neurons ◽  
Functional Markers ◽  
Kinase Signaling ◽  
Astrocyte Activation ◽  
Transcriptional Responses

AbstractParkinson’s disease (PD) is a neurodegenerative disorder characterized by the death of midbrain dopamine neurons. The pathogenesis of PD is poorly understood, though misfolded and/or aggregated forms of the protein α-synuclein have been implicated in several neurodegenerative disease processes, including neuroinflammation and astrocyte activation. Astrocytes in the midbrain play complex roles during PD, initiating both harmful and protective processes that vary over the course of the disease. However, despite their significant regulatory roles during neurodegeneration, the cellular and molecular mechanisms that promote pathogenic astrocyte activity remain mysterious. Here, we show that α-synuclein preformed fibrils (PFFs) induce pathogenic activation of human midbrain astrocytes, marked by inflammatory transcriptional responses, downregulation of phagocytic function, and conferral of neurotoxic activity. These effects required the necroptotic kinases RIPK1 and RIPK3, but were independent of MLKL and necroptosis. Instead, both transcriptional and functional markers of astrocyte activation occurred via RIPK-dependent activation of NF-κB signaling. Our study identifies a previously unknown function for α-synuclein in promoting neurotoxic astrocyte activation, as well as new cell death-independent roles for RIP kinase signaling in the regulation of glial cell biology and neuroinflammation. Together, these findings highlight previously unappreciated molecular mechanisms of pathologic astrocyte activation and neuronal cell death with implications for Parkinsonian neurodegeneration.

scholarly journals Ozone responses in Arabidopsis: beyond stomatal conductance

2021 ◽  
Author(s):  
Luis O Morales ◽  
Alexey Shapiguzov ◽  
Omid Safronov ◽  
Johanna Leppälä ◽  
Lauri Vaahtera ◽  
...  
Keyword(s):  
Cell Death ◽  
Tropospheric Ozone ◽  
Natural Variation ◽  
Air Pollutant ◽  
Plant Responses ◽  
Negative Effects ◽  
Transcriptional Responses ◽  
Physiological Mechanisms ◽  
Future Studies ◽  
Key Parameter

Abstract Tropospheric ozone (O3) is a major air pollutant that decreases yield of important crops worldwide. Despite long-lasting research of its negative effects on plants, there are many gaps in our knowledge on how plants respond to O3. In this study, we used natural variation in the model plant Arabidopsis (Arabidopsis thaliana) to characterize molecular and physiological mechanisms underlying O3 sensitivity. A key parameter in models for O3 damage is stomatal uptake. Here we show that the extent of O3 damage in the sensitive Arabidopsis accession Shahdara (Sha) does not correspond with O3 uptake, pointing toward stomata-independent mechanisms for the development of O3 damage. We compared tolerant (Col-0) versus sensitive accessions (Sha, Cvi-0) in assays related to photosynthesis, cell death, antioxidants, and transcriptional regulation. Acute O3 exposure increased cell death, development of lesions in the leaves, and decreased photosynthesis in sensitive accessions. In both Sha and Cvi-0, O3-induced lesions were associated with decreased maximal chlorophyll fluorescence and low quantum yield of electron transfer from Photosystem II to plastoquinone. However, O3-induced repression of photosynthesis in these two O3-sensitive accessions developed in different ways. We demonstrate that O3 sensitivity in Arabidopsis is influenced by genetic diversity given that Sha and Cvi-0 developed accession-specific transcriptional responses to O3. Our findings advance the understanding of plant responses to O3 and set a framework for future studies to characterize molecular and physiological mechanisms allowing plants to respond to high O3 levels in the atmosphere as a result of high air pollution and climate change.

scholarly journals Yeast Nap1-Binding Protein Nbp2p Is Required for Mitotic Growth at High Temperatures and for Cell Wall Integrity

Genetics ◽  
2003 ◽  
Vol 165 (2) ◽  
pp. 517-529
Author(s):  
Kentaro Ohkuni ◽  
Asuko Okuda ◽  
Akihiko Kikuchi
Keyword(s):  
Cell Death ◽  
Cell Wall ◽  
High Temperature ◽  
High Temperatures ◽  
Hybrid System ◽  
Mapk Pathway ◽  
Binding Protein ◽  
Cell Wall Integrity ◽  
Calcofluor White ◽  
Two Hybrid

AbstractNbp2p is a Nap1-binding protein in Saccharomyces cerevisiae identified by its interaction with Nap1 by a two-hybrid system. NBP2 encodes a novel protein consisting of 236 amino acids with a Src homology 3 (SH3) domain. We showed that NBP2 functions to promote mitotic cell growth at high temperatures and cell wall integrity. Loss of Nbp2 results in cell death at high temperatures and in sensitivity to calcofluor white. Cell death at high temperature is thought not to be due to a weakened cell wall. Additionally, we have isolated several type-2C serine threonine protein phosphatases (PTCs) as multicopy suppressors and MAP kinase-kinase (MAPKK), related to the yeast PKC MAPK pathway, as deletion suppressors of the nbp2Δ mutant. Screening for deletion suppressors is a new genetic approach to identify and characterize additional proteins in the Nbp2-dependent pathway. Genetic analyses suggested that Ptc1, which interacts with Nbp2 by the two-hybrid system, acts downstream of Nbp2 and that cells lacking the function of Nbp2 prefer to lose Mkk1, but the PKC MAPK pathway itself is indispensable when Nbp2 is deleted at high temperature.

scholarly journals Survival Analysis by Penalized Regression and Matrix Factorization

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Yeuntyng Lai ◽  
Morihiro Hayashida ◽  
Tatsuya Akutsu
Keyword(s):  
Matrix Factorization ◽  
Regression Models ◽  
Nonnegative Matrix ◽  
B Cell Lymphoma ◽  
Penalized Regression ◽  
Survival Prediction ◽  
Suitable Model ◽  
Gene Expressions ◽  
Combination Methods ◽  
Survival Patterns

Because every disease has its unique survival pattern, it is necessary to find a suitable model to simulate followups. DNA microarray is a useful technique to detect thousands of gene expressions at one time and is usually employed to classify different types of cancer. We propose combination methods of penalized regression models and nonnegative matrix factorization (NMF) for predicting survival. We triedL1- (lasso),L2- (ridge), andL1-L2combined (elastic net) penalized regression for diffuse large B-cell lymphoma (DLBCL) patients' microarray data and found thatL1-L2combined method predicts survival best with the smallest logrankPvalue. Furthermore, 80% of selected genes have been reported to correlate with carcinogenesis or lymphoma. Through NMF we found that DLBCL patients can be divided into 4 groups clearly, and it implies that DLBCL may have 4 subtypes which have a little different survival patterns. Next we excluded some patients who were indicated hard to classify in NMF and executed three penalized regression models again. We found that the performance of survival prediction has been improved with lower logrankPvalues. Therefore, we conclude that after preselection of patients by NMF, penalized regression models can predict DLBCL patients' survival successfully.

Sign in / Sign up

Export Citation Format

Share Document