Short-term effects of Elastase inhibition on human islets protein phosphorylation
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE189986 | GEO | 2024/02/13
REPOSITORIES: GEO
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Project description:Short-term effects of Elastase inhibition on human islets protein phosphorylation
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Project description:To evaluate the long-term effect of elastase inhibition using telaprevir, sivelestat, or DMSO on human islet cells.
2024-02-13 | GSE190447 | GEO
Project description:Long-term effects of Elastase inhibition on human islets at single-cell resolution
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Project description:Microarray profiling using the Affymetrix GeneChip Human Genome U133 plus 2.0 arrays was performed to comprehensively determine global changes in transcript levels in bronchial epithelial cells following elastase treatment. Elastase caused a significant change in expression (P < 0.05, fold change 1.5) of 364 transcripts corresponding to 348 genes. Elastase affected the expression of signaling molecules including chemokines, cytokines, and receptors, as well as components of the spliceosome, transcription machinery, cell cycle and ubiquitin-mediated proteolysis. Importantly, the transcriptional response to elastase was attenuated by co-administration of 10 M-BM-5M symplostatin 5. Comparison of the global heatmap of significantly modulated transcripts indicated that symplostatin 5 potently prevented the global effects of elastase. Symplostatin 5 caused a 20M-bM-^@M-^S68 % reduction in transcript levels of elastase-inducible genes including those involved in NOD- and MAPK- signaling pathways which are relevant to inflammation. Four samples were analyzed in biological duplicates. Transcriptome profile of elastase, elastase+symplostatin 5 were compared to control.
2013-01-28 | E-GEOD-41600 | biostudies-arrayexpress
Project description:To investigate the function of neutrophil elastase in breast cancer metastasis, as a function of time We then performed gene expression profiling analysis using data obtained from PyMT tumors (N=5 each) that are either WT or knockout for Neutrophil Elastase i.e. NEKO.
2023-10-21 | GSE217980 | GEO
Project description:Single-cell RNA sequencing (scRNA-seq) was performed on the infrarenal abdominal aortas from C57BL/6J mice at days 7 and 14 post periadventitial elastase-induced AAA or days 14 post periadventitial heat-inactive elastase incubation. This study report the changes of cellular subpopulations, fractions and transcriptomic profiles in response to elastase-induced AAA model.
2020-10-07 | GSE152583 | GEO
Project description:Microarray profiling using the Affymetrix GeneChip Human Genome U133 plus 2.0 arrays was performed to comprehensively determine global changes in transcript levels in bronchial epithelial cells following elastase treatment. Elastase caused a significant change in expression (P < 0.05, fold change 1.5) of 364 transcripts corresponding to 348 genes. Elastase affected the expression of signaling molecules including chemokines, cytokines, and receptors, as well as components of the spliceosome, transcription machinery, cell cycle and ubiquitin-mediated proteolysis. Importantly, the transcriptional response to elastase was attenuated by co-administration of 10 µM symplostatin 5. Comparison of the global heatmap of significantly modulated transcripts indicated that symplostatin 5 potently prevented the global effects of elastase. Symplostatin 5 caused a 20–68 % reduction in transcript levels of elastase-inducible genes including those involved in NOD- and MAPK- signaling pathways which are relevant to inflammation.
2013-01-28 | GSE41600 | GEO
Project description:Purpose: The goal of this study is to address if in utero and early life nicotine exposure can prime the offspring to be more succetible to develop emphysema in adulthood Methods: A mouse model of two hits: a prenatal hit and a later insult delivered in adulthood was used in this study. In brief, Nicotine (200 mg/L) was supplied immediately after mating and administered to the females in drinking water supplemented with 2% saccharin for the whole period of gestation and until the post-natal day 16 (nicotine group). As a control, we used drinking water with 2% saccharin (control group). Pups born from nicotine-exposed or control mothers were intranasally instilled with elastase or saline at the age of 11 weeks and sacrificed at post-elastase day (ped) 21. Lungs were collected at ped21 and laser dissected to separate the emphysematous and normal-looking tissue from elastase-instilled lungs. The RNA was then extracted and submited to RNAseq analysis. We had 6 different groups: two for saline instilled animals (normal_control_saline (C-S), normal_nicotine-saline (N-S)), and for elastase-instilled animals we had 4 groups: 2 for emphysematous regions (emphysema_ControlElastase (eC-E) and emphysema_NicotineElastase(eN-E)) and 2 for normal regions (normal_ControlElastase(nC-E) and normal_NicotineElastase(nN-E)). Results: Nicotine upregulated zero and 46 genes and downregulated 2 and 29 in saline and elastase instilled respectivelly. Elastase upregulated zero and 3 and downregulated 1 and 1 genes in controls and nicotine-pretreated samples respectively. Pathway analysis performed with differentially expressed genes due to nicotine-pretreatment in elastase instilled animals with MetaCore software (https://portal.genego.com/) (fold change of 2 or more and p<0.05) revealed downregulation of the several immune system related pathways, gamma-secretase proteolitic pathway, ubiquitin-proteasomal pathway, notch signaling pathway and others. Conclusions: Our results identify the the early nicotine exposure as an important insult that affects the proteomic signature at ped21
2022-03-09 | GSE167568 | GEO
Project description:Obesity is closely associated with adipose tissue inflammation and insulin resistance. Dysglycemia and type 2 diabetes results when islet β cells fail to maintain appropriate insulin secretion in the face of insulin resistance. To clarify the early transcriptional events leading to β-cell failure in the setting of obesity, we fed male C57BL/6J mice an obesogenic, high fat diet (60% kcal from fat) or control diet (10% kcal from fat) for one week and islets from these mice (from 4 high fat- and 3 control-fed mice) were subjected to single cell RNA sequencing analysis. Islet endocrine cell types (α cells, β cells, δ cells, PP cells) and other resident cell types (macrophages, T cells) were annotated by transcript profiles and visualized using Uniform Manifold Approximation and Projection for Dimension Reduction (UMAP) plots. UMAP analysis revealed distinct cell sub-populations (11 for β cells, 5 for α cells, 3 for δ cells, PP cells, ductal cells, endothelial cells), emphasizing the heterogeneity of cell populations in the islet. We identified that distinct β cell populations downregulate genes associated with the endoplasmic reticulum stress response and upregulate genes associated with insulin secretion, while others upregulate genes that impair insulin secretion, cellular proliferation, and survival. Moreover, all β cell populations negatively regulate genes associated with immune response activation. Our data indicate that an early transcriptional response in islets to an obesogenic diet reflects an attempt by distinct populations of β cells to augment or impair cellular function, possible harbingers of ensuing insulin resistance.
2020-12-03 | GSE162512 | GEO
Project description:We single cell sequenced multiplexed primary human islets treated ex vivo with ER and inflammatory chemicals, indexed cell type specific stress responses, found genes to regulate in SC-islets to reduce apoptosis. We conducted multiomic ATAC+RNA sequencing on human islets treated with BFA, DMSO, IL1B+IFNG+TNFa, or PBS
2024-05-06 | GSE237448 | GEO