Long-term effects of Elastase inhibition on human islets at single-cell resolution
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE190447 | GEO | 2024/02/13
REPOSITORIES: GEO
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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.
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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.
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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:Purpose: The goal of this study is to address if in utero and early life nicotine exposure can affect genetic profile in early ephysema 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) 3. Whole lung were collected at ped3 and total RNA was sequenced. We had 4 different groups: control_saline (C-S), control_elastase (C-E), nicotine_saline (N-S) and nicotine_elastase (N-E). ALl the groups had 3 replicas, except N-E group that had 5 different replicas. Results: At ped3 nicotine upregulated 219 and 2 and downregulated 2 and 109 genes in saline and elastase-instilled samples respectively. Elastase upregulated 723 and 439 and downregulated 116 and 77 genes in controls and nicotine-pretreated samples respectively. Pathway analysis performed with MetaCore software (https://portal.genego.com/) (fold change of 2 or more and p<0.05) revealed many identical pathway activated by elastase instillation in both controls and nicotine-pretreated samples such as the cell cycle, DNA damage and cell adhesion, but also revieled the main difference in activation of the immune system between the controls and nicotine-pretreated samples. Conclusions: Our results identify the the early nicotine exposure as an important insult that affects the proteomic signature at ped3
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Project description:In this study we show, for the first time, that whole islets can be cultured and significantly expanded long-term in vitro on specific basement membrane (BM) laminin LN-521 which is a normal component of islet BMs. Isolated islets adhere and flatten to form 2-3 cell layer entities with ~10 % of all endocrine cell types proliferating after 2-5 weeks in culture. Time-lapse imaging of freshly isolated islets in suspension labeled with hypoxia and DNA degradation indicators reveals that spherical islets on LN-111 rapidly develop hypoxia and central necrosis, in contrast to islets attached to LN-521, which normal b-cell glucose responsiveness. RNA sequencing analyses reveal that freshly isolated islets express LN-521 binding integrins. Compared to other matrices, islets grown on LN-521 develop a unique expression signature, including expression of specific integrins, involved in cell adhesion and matrix production as well as proliferation. The results reveal specific LN-521-mediated effects into islet cells and suggest that use of in vitro expanded islets may significantly enhance the efficacy of islet transplantation treatment of T1D.
2018-11-09 | GSE89677 | GEO