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opencc-by-4.0Apr 2022View details →

Lipogenesis mediated by OGR1 regulates metabolic adaptation to acid stress in cancer cells via autophagy

Malignant tumors exhibit altered metabolism resulting in a highly acidic extracellular microenvironment. Here we show that cytoplasmic lipid droplet (LD) accumulation, indicative of a lipogenic phenotype is a cellular adaption to extracellular acidity. LD marker PLIN2, is strongly associated with poor overall survival in breast cancer patients. Acid-induced LD accumulation is triggered by activation of the acid-sensing GPCR, OGR1 expressed highly in breast tumors. OGR1 depletion inhibited acid induced lipid accumulation while activation by synthetic agonist triggered LD formation. Inhibition of OGR1 downstream signaling abrogated the lipogenic phenotype which could be rescued with OGR1 ectopic expression. OGR1 depleted cells showed growth inhibition under acidic growth conditions in vitro and tumor formation in vivo. Isotope tracing showed that the source of lipid precursors is primarily autophagy-derived ketogenic amino acids. OGR1 depleted cells were defective in endoplasmic reticulum stress response and autophagy, hence failed to accumulate LDs affecting survival under acidic stress.

opencc-by-4.0Apr 2022View details →

Accelerated Stress Tests for Solid Oxide Cells via Artificial Aging of the Fuel Electrode

AD ASTRA: Data from Experiments for Artificial Aging of the Fuel Electrode in Solid Oxide Cells  via Redox Cycling One of the big hurdles towards fast deployment of Solid Oxide Cells (fuel cells or electrolyzers) is durability. Although intensive works are carried out for life time improvement, they meet a serious problem concerning long term electrochemical tests for accumulation of reliable data that may continue several years, which is unaffordable. A problem-solving approach is the introduction of Accelerated Stress Tests (AST) applying  high levels of stress for a shorter period thus reducing the test time for degradation qualification. Since there are no definite criteria for the level of acceleration of a specific degradation phenomenon, the selection of aggravating conditions is a critical moment which is under studies in the FCH JU Project AD ASTRA (GA 825027). Herein we present data accumulated during the development of a procedure for artificial accelerated aging of the fuel electrode via redox cycling. They include electrochemical testing (current-voltage curves and impedance measurements) and microstructural characterization (SEM-BSE image analysis), as well as procedure for redox cycling.

opencc-by-4.0Sep 2022View details →

ETV6 represses Tumor Necrosis Factor During Stress Hematopoiesis to Regulate Mouse Stem Cell Function

At the root of the blood system lies a heterogenous population of hematopoietic stem and progenitor cells (HSPCs), which reside in the bone marrow (BM) and give rise to diverse blood lineages. Maintaining this pool of self-renewing HSPCs is critical to uphold hematopoiesis during period of stress such as bleeding or infection1. ETS Variant Transcription Factor 6 (ETV6) is a transcriptional repressor that is highly expressed in HSPCs2 where it is essential for development and maintenance of the adult hematopoiesis 3. In 2015, our group4 and others5-7  identified germline pathogenic ETV6 variants in families with predisposition to B-acute lymphoblastic leukemia (B-ALL) and thrombocytopenia, defining a new genetic syndrome known as Thrombocytopenia 5 (T5). Subsequently, we performed targeted germline ETV6 sequencing of remission blood samples from over 4,000 children with B-ALL and identified germline ETV6 variants in ~1% of cases7. In vitro studies revealed that ETV6 variant proteins exhibit impaired repressor activity, reduced DNA binding, and aberrant subcellular localization4,5,7,8. Overall, these studies indicated that T5-associated germline ETV6 variants negatively impact the repressor activity of ETV6. In support of this notion, transcriptional profiling of peripheral blood cells from T5 patients has revealed upregulation of interferon response genes9. Nevertheless, little remains known about the mechanisms by which ETV6 regulates the HSPC compartment and how T5-associated ETV6 variants contribute to disease.   To address these questions, we used CRISPR-Cas9 gene editing to generate a novel mouse model harboring a pathogenic heterozygous germline Etv6 variant, R355X, the murine equivalent to the human T5-associated variant R359X10. Through the comprehensive study of this model, we describe a novel role for ETV6 during aging and regenerative hematopoiesis and show that the heterozygous Etv6R355X variant impairs HSC function in vitro and in vivo. Using genomic approaches to interrogate mouse and human HSCs, we identify new ETV6 targets, including the gene encoding Tumor Necrosis Factor (TNF) and genes involved in TNF signaling. Further, we show increased TNF production and cell cycling in Etv6R355X/+ mouse HSPCs post-BM transplantation. Finally, we demonstrate that genetic ablation of Tnf restores the long-term potential of Etv6R355X/+ cells in serial replating assays in vitro. Together, these findings provide novel insights into the pathways regulated by ETV6 and demonstrate how a pathogenic variant impacts ETV6 function in the context of hematopoietic stress. All bulk RNAseq, Cut&Run, ATACseq, and Hi-C data has been submitted to in the Gene Expression Omnibus (accession number GSE213597) and Sequence Read Archive (BioProject number PRJNA880871). Due to the journal’s limitation on submitted supplementary data  as an Excel file, all post-analysis supplemental data files are deposited in Dryad data repository to be made available with this manuscript.

opencc-by-4.0Aug 2024View details →

Dataset to: Realistic accelerated stress tests for PEM fuel cells: Test procedure development based on standardized automotive driving cycles

This is the dataset to the published article "Realistic accelerated stress tests for PEM fuel cells: Test procedure development based on standardized automotive driving cycles" (DOI: 10.1016/j.ijhydene.2023.08.292) in which the degradation of two commercial PEM fuel cell stacks was analyzed. Please cite this publication if you use the dataset in a publication as follows: P. Thiele, Y. Yang, S. Dirkes, M. Wick, S. Pischinger, Realistic accelerated stress tests for PEM fuel cells: Test procedure development based on standardized automotive driving cycles, Int. J. Hydrogen Energy 52 (Part D) (2024) 1065–1080, https://doi.org/10.1016/j.ijhydene.2023.08.292.

opencc-by-4.0Sep 2019View details →

Processed data for "Dissociation of solid tumour tissues with cold active protease for single-cell RNA-seq minimizes conserved collagenase-associated stress responses"

tar.gz of processed data in the form of compressed R files (rds) of SingleCellExperiment (<a href="https://bioconductor.org/packages/release/bioc/html/SingleCellExperiment.html">https://bioconductor.org/packages/release/bioc/html/SingleCellExperiment.html</a>) objects and a metadata csv for the data in the publication Dissociation of solid tumour tissues with cold active protease for single-cell RNA-seq minimizes conserved collagenase-associated stress responses (O'Flanagan et al. 2019).

opencc-zeroDec 2017View details →

Data from: Response to persistent er stress in plants: a multiphasic process that transitions cells from prosurvival activities to cell death

The unfolded protein response (UPR) is a highly conserved response that protects plants from adverse environmental conditions. The UPR is elicited by endoplasmic reticulum (ER) stress, in which unfolded and misfolded proteins accumulate within the ER. Here, we induced the UPR in maize (Zea mays) seedlings to characterize the molecular events that occur over time during persistent ER stress. We found that a multiphasic program of gene expression was interwoven among other cellular events, including the induction of autophagy. One of the earliest phases involved the degradation by regulated IRE1-dependent RNA degradation (RIDD) of RNA transcripts derived from a family of peroxidase genes. RIDD resulted from the activation of ZmIRE1 for promiscuous ribonuclease activity that attacks the mRNAs of secreted proteins. This was followed by an upsurge in expression of the canonical UPR genes indirectly driven by ZmIRE1 due to its splicing of Zmbzip60 to make an active transcription factor that directly upregulates many of the UPR genes. At the peak of UPR gene expression, a global wave of alternative RNA processing led to the production of many aberrant UPR gene transcripts, likely tempering the ER stress response. During later stages of ER stress, ZmIRE1's activity declined as did the expression of survival modulating genes, Bax inhibitor1 and Bcl-2-associated athanogene7, amidst a rising tide of cell death. Thus, in response to persistent ER stress, maize seedlings embark on a course of gene expression and cellular events progressing from adaptive responses to cell death.

opencc-by-4.0Dec 2023View details →

Single-Cell RNA-Sequencing Reveals Placental Response under Environmental Stress

This repository provides scRNA-seq data corresponding to the manuscript "Single-Cell RNA-Sequencing Reveals Placental Response under Environmental Stress" by Van Buren, Azzara, Rangel-Moreno, de la Luz Garcia-Hernandez, Murphy, Cohen, Lin, and Park. The repository includes both count by gene matrices output from CellRanger version 6.0.1 (file names *_filtered_feature_matrix.h5 for each of the eight samples Control_1_M, Control_1_F, Control_2_M, Control_2_F, As_1_M, As_1_F, As_2_M, As_2_F), and a finalized Seurat object including cell type assignments as used for analyses in the manuscript (file name final_Seurat_obj.RData). Accompanying code used in analysis can be found at https://github.com/edvanburen/placenta_code.

opencc-zeroJan 2024View details →

Data from: anterior pituitary transcriptomics following a high fat diet: impact of oxidative stress on cell metabolism

Anterior pituitary cells are highly active with regards to protein synthesis and secretion, processes which depend heavily on mitochondrial ATP production and functional endoplasmic reticula. It is well known that obesity adds an allostatic overload to tissues, requiring them to adapt to inflammation and oxidative stress. Therefore, we hypothesized that the pituitary is highly vulnerable to the stress of high fat diet-induced weight gain. In this study, we utilized a 10-15 week high fat diet (HFD, 60%) plus a thermoneutral housing paradigm, testing both male and female FVB.129P mice. We quantified serum hormones and cytokines, characterized the metabolic phenotype, and defined changes in the pituitary transcriptome using single-cell RNA-seq. Weight gain was significant by 3 weeks in HFD mice, and by 10 weeks all HFD groups had gained 20 g. HFD females (15 weeks) had increased energy expenditure and decreased activity. All HFD groups showed increases in serum leptin, Il-6, resistin, MCP-1, and TNFα. HFD males had increased insulin; both HFD males and females had increased TSH, and HFD females had decreased serum prolactin and growth hormone (GH) pulse amplitude. Pituitary scRNA-seq revealed modest or no changes in pituitary cell gene expression in the different cell types from HFD males after 10 or 15 weeks or HFD females after 10 weeks. However, females exposed to a HFD for 15 weeks showed significant numbers of differentially expressed genes in lactotropes and stem cells. Pathway analyses identified a reduction in pathways that supported protein translation, ribosome biogenesis, and oxidative phosphorylation, indicating mitochondrial dysfunction. Collectively, these studies reveal that pituitary cells from males are more resilient to the oxidative stress of obesity than females and identify the most vulnerable pituitary cell populations in females.

opencc-by-4.0Jan 2023View details →

Linear contraction of stress fibers generates cell body rotation

Raw image data and numerical data used to generate plots and graphs included in the manuscript. Raw sequential images to make supplementary movies.

opencc-by-4.0Dec 2021View details →

Molecular dynamics of solids at constant pressure and stress using anisotropic stochastic cell rescaling - dataset

Supporting data related to manuscript "Molecular dynamics at constant pressure and stress using anisotropic stochastic cell rescaling"

opencc-by-4.0Aug 2022View details →

The effect of antidepressants on genes of endoplasmic reticulum stress in human astrocyte cell line.

Many central nervous system (CNS) diseases, including major depressive disorder (MDD), are underpinned by the unfolded protein response (UPR) activated under endoplasmic reticulum (ER) stress. New, more efficient, therapeutic options for MDD are needed to avoid adverse effects and drug resistance. Therefore, the aim of the work was to determine whether UPR signalling pathway activation in astrocytes may serve as a novel target for antidepressant drugs. Among the tested antidepressants (escitalopram, amitriptyline, S-ketamine), only S-ketamine induced the expression of most ER stress-responsive genes in astrocytes. <a href="https://doi.org/10.3390/pharmaceutics14040846">https://doi.org/10.3390/pharmaceutics14040846</a>

opencc-by-4.0Aug 2024View details →

Chronic social defeat stress induces meningeal neutrophilia via type I interferon signaling: single cell RNA sequencing data

Meningeal single cell RNA sequencing data Meningeal samples were collected from both dorsal and ventral skull, avoiding inclusion of choroid plexus. Samples were digested in 2.5 mg/mL Collagenase D (Cat. #11088858001; Roche) and 12.5 μL of 0.5 mg/mL DNAseI (Cat. #L5002139; Worthington), put on a shaker at 370C for 30 m, diluted with cold HBSS + 0.1% BSA, and mashed through a 70 μm cell strainer prior to sorting. Data represent live, nucleated, singlet cells (DAPI-DRAQ5+) sorted on a BD FACS Aria Fusion into HBSS + 10% FBS prior to droplet encapsulation using 10x Genomics’ Drop-seq platform (Chromium v2). 10X chip lane is indicate by 'group' column Group 1 = 4 pooled homecage control (unstressed) mice Group 2 = 4 pooled homecage control (unstressed) mice Group 3 = 4 pooled mice exposed to chronic social defeat for 14 days; tissue was collected 2 hours following final defeat See the following repositories for data processing: <a href="https://github.com/maryellenlynall/2019_bcell_stress/blob/master/bcellstress20.Rmd">https://github.com/maryellenlynall/2019_bcell_stress/</a> (processing from raw files starts at bcellstress020.Rmd) <a href="https://github.com/staceykigar/meningeal_neut/">https://github.com/staceykigar/meningeal_neut/</a> We also provide a processed dataset (processed.RData) with assays 'counts' and 'logcounts' which is the processed single cell object saved at line "# Save object for upload to Zenodo" in script <a href="https://github.com/staceykigar/meningeal_neut/">https://github.com/staceykigar/meningeal_neut/</a>neutrophilstress01.Rmd  Cluster annotations are in sce$Annotation Neutrophil subcluster annotations are in sce$Subcluster Sample condition is in sce$cond, where "HC" indicates homecage control and "SD" indicates chronic social defeat 10X chip lane is in sce$group

opencc-zeroAug 2023View details →

Data from: The CST complex facilitates cell survival under oxidative genotoxic stress

Genomic DNA is constantly exposed to a variety of genotoxic stresses, and it is crucial for organisms to be equipped with mechanisms for repairing the damaged genome. Previously, it was demonstrated that the mammalian CST (CTC1-STN1-TEN1) complex, which was originally identified as a single-stranded DNA-binding trimeric protein complex essential for telomere maintenance, is required for survival in response to hydroxyurea (HU), which induces DNA replication fork stalling. It is still unclear, however, how the CST complex is involved in the repair of diverse types of DNA damage induced by oxidizing agents such as H2O2. STN1 knockdown (KD) sensitized HeLa cells to high doses of H2O2. While H2O2-induced DNA strand breaks throughout the cell cycle, STN1 KD cells were as resistant as control cells to H2O2 treatment when challenged in the G1 phase of the cell cycle, but they were sensitive when exposed to H2O2 in S/G2/M phase. STN1 KD cells showed a failure of DNA synthesis and RAD51 foci formation upon H2O2 treatment. Chemical inhibition of RAD51 in shSTN1 cells did not exacerbate the sensitivity to H2O2, implying that the CST complex and RAD51 act in the same pathway. Collectively, our results suggest that the CST complex is required for maintaining genomic stability in response to oxidative DNA damage, possibly through RAD51-dependent DNA repair/protection mechanisms.

ClinicalTrials.gov36/100

Effect of Statins on Oxidative Stress and Endothelial Progenitor Cells

ClinicalTrials.gov study NCT00166036. IPD Sharing: Not stated. Countries: 1. Publications: 1.

restrictedIPD-UNDECIDEDFeb 2026View details →

ClinicalTrials.gov36/100

Effect of Nebivolol on Oxidative Stress and Endothelial Progenitor Cells

ClinicalTrials.gov study NCT01041287. IPD Sharing: Not stated. Countries: 1. Publications: 1.

restrictedIPD-UNDECIDEDFeb 2026View details →

ClinicalTrials.gov36/100

Autologous Muscle Derived Cells Female Stress Urinary Incontinence Clinical Study

ClinicalTrials.gov study NCT01382602. IPD Sharing: Not stated. Countries: 3. Publications: 1.

restrictedIPD-UNDECIDEDFeb 2026View details →

publicAug 2023View details →

Data from: The CST complex facilitates cell survival under oxidative genotoxic stress

Open the record for dataset details and reuse information.

publicMay 2025View details →

Sensing of extracellular L-Proline availability by the integrated stress response determines the outcome of cell competition

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