Identification of inflammatory genes suppressed by heat shock
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE16266 | GEO | 2009/12/21
SECONDARY ACCESSION(S): PRJNA115107
REPOSITORIES: GEO
Similar Datasets
Project description:To clarify inflammatory genes whose expression is suppressed at high temperatures, we performed comprehensive analysis of gene expression by using a DNA microarray. Two independent primary cultures of mouse embryo fibroblasts (MEF1 and MEF2) were treated with LPS for 4 hours, or treated with LPS for 4 hours after the pretreatment with heat shock at 42ËC for 1 hour, and we identified 100 genes that undergo more than a 3-fold increase with LPS treatment. Remarkably, 86 genes (86%) underwent less than a 2-fold increase after combined treatments with heat shock and LPS in MEF1 and MEF2 cells. Experiment Overall Design: Total RNAs were prepared from two primary cultures of mouse embryo fibroblasts (MEF) derived from two independent embryos at embryonic day 15.5 (ICR mice). Cells were maintained at 37ËC (Control), treated with lipopolysaccharide (LPS, E. coli 0127:B8, Sigma, 1 μg/ml) for 4 hours, or treated with LPS for 4 hours after the pretreatment of heat shock at 42ËC for 1 hour. Gene expression was analyzed by using GeneChip Mouse Genome 430 2.0 Array (Affymetrix, Santa Clara, CA).
2010-01-19 | E-GEOD-16266 | biostudies-arrayexpress
Project description:The concentrations and copy number of proteins in the mouse Bone Marrow Derived proteome was determined for control, 10 ng/mL LPS stimulation, and LPS stimulation plus the addition of 100 nM dexamethasone, after an incubation for 24 hours and with four biological replicates for each condition. Over 6000 proteins were detected, 410 of which were upregulated by LPS (> 1.5-fold increase, adjusted p value < 0.05). 125 of these LPS-induced proteins were significantly regulated by Dexamethason > 1.5 fold 899 increase or decrease, adjusted p value <0.05).
2024-01-26 | PXD041375 | Pride
Project description:Proctor2005 - Actions of chaperones and their
role in ageing
This model is described in the article:
Modelling the actions of
chaperones and their role in ageing.
Proctor CJ, Soti C, Boys RJ,
Gillespie CS, Shanley DP, Wilkinson DJ, Kirkwood TB.
Mech. Ageing Dev. 2005 Jan; 126(1):
119-131
Abstract:
Many molecular chaperones are also known as heat shock
proteins because they are synthesised in increased amounts
after brief exposure of cells to elevated temperatures. They
have many cellular functions and are involved in the folding of
nascent proteins, the re-folding of denatured proteins, the
prevention of protein aggregation, and assisting the targeting
of proteins for degradation by the proteasome and lysosomes.
They also have a role in apoptosis and are involved in
modulating signals for immune and inflammatory responses.
Stress-induced transcription of heat shock proteins requires
the activation of heat shock factor (HSF). Under normal
conditions, HSF is bound to heat shock proteins resulting in
feedback repression. During stress, cellular proteins undergo
denaturation and sequester heat shock proteins bound to HSF,
which is then able to become transcriptionally active. The
induction of heat shock proteins is impaired with age and there
is also a decline in chaperone function. Aberrant/damaged
proteins accumulate with age and are implicated in several
important age-related conditions (e.g. Alzheimer's disease,
Parkinson's disease, and cataract). Therefore, the balance
between damaged proteins and available free chaperones may be
greatly disturbed during ageing. We have developed a
mathematical model to describe the heat shock system. The aim
of the model is two-fold: to explore the heat shock system and
its implications in ageing; and to demonstrate how to build a
model of a biological system using our simulation system
(biology of ageing e-science integration and simulation
(BASIS)).
This model is hosted on
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BIOMD0000000091.
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2024-09-02 | BIOMD0000000091 | BioModels
Project description:Environmental stress, such as oxidative or heat stress, induces the activation of the heat shock response
(HSR) and leads to an increase in the heat shock proteins (HSPs) level. These HSPs act as molecular
chaperones to maintain cellular proteostasis. Controlled by highly intricate regulatory mechanisms,
having stress-induced activation and feedback regulations with multiple partners, the HSR is still
incompletely understood. In this context, we propose a minimal molecular model for the gene
regulatory network of the HSR that reproduces quantitatively different heat shock experiments both
on heat shock factor 1 (HSF1) and HSPs activities. This model, which is based on chemical kinetics
laws, is kept with a low dimensionality without altering the biological interpretation of the model
dynamics. This simplistic model highlights the titration of HSF1 by chaperones as the guiding line of
the network. Moreover, by a steady states analysis of the network, three different temperature stress
regimes appear: normal, acute, and chronic, where normal stress corresponds to pseudo thermal
adaption. The protein triage that governs the fate of damaged proteins or the different stress regimes
are consequences of the titration mechanism. The simplicity of the present model is of interest in
order to study detailed modelling of cross regulation between the HSR and other major genetic
networks like the cell cycle or the circadian clock.
Sivéry, A., Courtade, E., Thommen, Q. (2016). A minimal titration model of the mammalian dynamical heat shock response. Physical biology, 13(6), 066008.
2022-01-25 | MODEL2201210001 | BioModels
Project description:High-temperature stress is a critical environmental parameter for all organisms and induces a cellular heat shock response, characterized by an upregulation of heat shock proteins. For Crenarchaeota, it is unknown how this response is regulated, given the lack of conservation of known prokaryotic or eukaryotic heat shock-regulating transcription factors and how cellular processes are affected. To this end, we studied the heat shock response of the thermoacidophilic Sulfolobus acidocaldarius, thriving in volcanic hot springs at 75°C, upon shift to 86°C, at the transcriptome and proteome level. By pulse-labeling of neosynthesized RNA and proteins upon heat shock, we show a drastic reduction of the cell’s major transcriptional activity immediately after shift and neosynthesis of certain abundant (heat shock) proteins, including the thermosome. By combining RNA-sequencing and mass spectrometry, we show that RNA levels of half of the genes are affected immediately after temperature shift and that reprogramming of the protein landscape takes at least one hour and changes are more subtle. Correlation analysis provides evidence that considerable post-transcriptional and post-translational regulation is occurring upon heat shock. Functional enrichment analysis indicates that nearly all biological processes are affected by heat shock. An overall downregulation is observed for transcription, translation, DNA replication and cell division. However, quality control of translation and of the protein landscape is increased. Many DNA repair pathways are differentially expressed, accompanied with an increase in a DNA import system. Furthermore, expression of DNA topoisomerases is investigated, coinciding with a significant differential expression of nucleoid-associated proteins. Based on these findings and considering the absence of a conserved DNA-binding motif, we propose that regulation of the heat shock response in Sulfolobales is most likely not established by a classical transcription factor, but is rather caused by changes in chromosome organization or established at the post-transcriptional level.
2023-08-07 | PXD038744 | Pride
Project description:RNA-Seq analysis of adult mouse cultured utricles exposed to 43C heat shock for 30 minutes and recovered for 2 hours in order to generate a heat shock signature for cultured mouse inner ear tissue
2018-12-31 | GSE116515 | GEO
Project description:FBXW7 modulates stress response by post-translational modification of HSF1 HSF1 orchestrates the heat-shock response upon exposure to heat stress and activates a transcriptional program vital for cancer cells. Genes positively regulated by HSF1 show increeased expression during heat shock while their expression is reduced during recovery. Genes negatively regulated by HSF1 show the opposite pattern. In this study we utilized the HCT116 FBXW7 KO colon cell line and its wild type counterpart to monitor gene expression changes during heat shock (42oC, 1 hour) and recovery (37oC for 2 hours post heat shock) using RNA sequencing. These results revealed that the heat-shock response pathway is prolonged in cells deficient for FBXW7.
2015-02-20 | GSE57397 | GEO
Project description:Direct comparison of the genome-level expression patterns of THP-1 cells exposed to either LPS or heat shock; Peripheral blood mononuclear cells (PBMC) serve a sentinel role allowing the host to efficiently sense and adapt to the presence of danger signals. Herein we have directly compared the genome-level expression patterns (microarray) of human PBMC (THP-1 cells) subjected to one of two canonical danger signals, heat shock and lipopolysaccharide (LPS). Based on sequential expression and statistical filters, and in comparison to control cells, we found that 3,988 genes were differentially regulated in THP-1 cells subjected to LPS stress, and 2,921 genes were differentially regulated in THP-1 cells subjected to heat shock stress. Venn analyses demonstrated that the majority of differentially regulated genes (greather than or equal to 70%) were uniquely expressed in response to one of the two danger signals. Functional analyses demonstrated that the two danger signals induced expression or repression of genes corresponding to unique pathways, molecular functions, biological processes, and gene networks. In contrast, there were 184 genes that were commonly upregulated by both stress signals, and 430 genes that were commonly downregulated by both stress signals. Interestingly, the 184 commonly upregulated genes corresponded to a gene network broadly related to inflammation, and more specifically to chemokine signaling. These data demonstrate that the mononuclear cell responses to the canonical stress signals, heat shock and LPS, are highly divergent. However, there is a heretofore unrecognized common pattern of gene network expression corresponding to chemokine-related biology. The data also serve as a reference database for investigators in the field of stress signaling. Experiment Overall Design: In vitro exposure of THP-1 cells to control conditions, LPS (1 micogram/ml for 4 hrs), or heat shock (43 deg C for 1 hour, followed by a 4 hour recovery at 37 deg C)
2008-06-20 | E-GEOD-9916 | biostudies-arrayexpress
Project description:Intra Peritoneal Chemo Hyperthermia (IPCH) is a recently validated option for the treatment of peritoneal carcinomatosis from colorectal or ovarian origin. This therapeutic program demonstrated a significant improvement of the late stages (i.e. carcinomatosis) of the disease. From a clinical point of view, within the first 24 hours after IPCH, patients undergo a systemic inflammatory response syndrome, and therefore require to be monitored in an intensive care unit. From a metabolic perspective, preliminary data have been shown a significant "anaerobic style" disturbance of energetic metabolism, suggesting a deep cellular energetic deficit throughout IPCH process.
Putative contradictory effects of IPCH, like the increase of chemotherapy-related cellular toxicity due to heat and on the other hand the initiation of a stress protein response (heat shock response) which helps to reduce the cell injuries, leads to conduct a research project on the underlying mechanisms: consequences, in terms of patient’s care and follow-up, are of high relevance.
The primary goal is a multimodal assessment of the IPCH-related cell modifications: signaling pathways, apoptosis and antitumoral immune response.
The assessment criteria include Heat shock protein expression (blood/cell ratio) compared to baseline values, apoptosis and immune response before/after IPCH.
The scheduled sample size is 30 patients having an IPCH and 30 patients contraindicated per surgery.
| 2131952 | ecrin-mdr-crc
Project description:gene expression was measured in five independent heat resistance selected replicate lines and five control lines. The genetic architecture underlying heat resistance remains partly unclear despite the well documented involvement of heat shock proteins (Hsps). It was previously shown that factors besides Hsps are likely to play an important role for heat resistance. In this study, gene expression arrays were used to make replicate measurements of gene expression before and up to 64h after a mild heat stress treatment, in flies selected for heat resistance and unselected control flies, to identify genes differentially expressed in heat resistance selected flies. We found 108 genes upregulated and 10 downregulated using the Affymetrix gene expression platform. Among the upregulated genes, a substantial number are involved in the phototransduction process. Another group of genes upregulated in selected flies is characterized by also responding to heat shock treatment several hours after peak induction of known Hsps revert to non-stress levels. These findings suggest phototransduction genes to be critically involved in heat resistance, and support a role for components of the phototransduction process in stress sensing mechanisms. In addition the results suggest yet uncharacterized genes responding to heat stress several hours after treatment to be involved in heat stress resistance. These findings mark an important increase in the understanding of heat resistance. Keywords: control versus selected
2006-08-01 | GSE5146 | GEO