Comprisons of lung tissue gene expression from AKR and C57BL/6 mice exposed to Cigarette smoke and LPS in ARDS/ALI mice model
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA798627 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Our previous study showed that AKR and C57BL/6 mice to cigarette smoke increased lipopolysaccharide (LPS)- induced increased lung vascular permeability. Viremic AKR mice were more susceptible to LPS-induced ALI than C57 on prolonged exposure. In this study we compared the global gene expression patterns to determine the genetic basis for the strain dependent responses to cigarette smoke and LPS-induced ALI. We found AKR transcriptomic responses didnot overlap with C57 mice and AKR mice showed increased responses compared to C57 mice. Global gene expression analysis using microarray was used to dermine the mechanisms of strain dependent responses to cigarette smoking and LPS mediated ALI
2023-05-28 | GSE193958 | GEO
Project description:The Acute Respiratory Distress Syndrome (ARDS)/Acute Lung Injury (ALI) was described 30 years ago, yet the interaction between specific sets of genes involved in this syndrome remains incompletely understood. Experiment Overall Design: 13 patients with ALI + sepsis and 21 patients with sepsis alone were recruited from the Medical Intensive Care Unit of the University of Pittsburgh Medical Center between February 2005 and June 2007. Whole blood was obtained from each patient within 48 hours of admission, and RNA was extracted for gene expression profiling, and comparison analysis.
2008-04-09 | E-GEOD-10474 | biostudies-arrayexpress
Project description:Endothelial cells (ECs) serve as a semipermeable barrier and play a key role in acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). It is well known that fibroblast growth factor receptor 1 (FGFR1) is a requirement for maintaining vascular integrity. However, how endothelial FGFR1 exerts its function remains obscure in ALI/ARDS. Here, we performed RNA-seq analysis to investigate transcriptional changes of ECs between saline and LPS group, WT (Fgfr1loxp/loxp) and endothelial Fgfr1-conditional knock out mice (Fgfr1iΔEC/iΔEC mice).
2023-03-29 | GSE216635 | GEO
Project description:ALI is one of the most common disease processes in adult and pediatric intensive care units and results in significant morbidity and mortality. The pathophysiology of ALI begins with a massive pro-inflammatory response likely mediated by as yet uncharacterized platelet/endothelium interactions with macrophage activation. This leads to a cytokine/chemokine cascade producing endothelial disruption. Neutrophilic infiltration of the alveolar wall and alveolar space with a concomitant procoagulant state develops. Despite the fact that inadequate understanding of ALI pathophysiology remains a barrier to effective treatment, novel therapeutics including ventilatory manipulations and anti-inflammatory molecules are beginning to improve the morbidity and mortality associated with this disease process. Keywords: Time Series Design, ALI - acute lung injury, ARDS - acute respiratory distress syndrome
2008-02-02 | GSE10361 | GEO
Project description:Increased fat intake is associated with obesity and insulin resistance. In some individuals, a failure of pancreatic b-cells to increase insulin production in response to the high demands of obesity leads to diabetes. We sought to determine whether the impaired b- cell adaptation in obesity is associated with differential expression of genes involved in b-cell expansion and intermediary metabolism. Two strains of inbred mice prone to obesity, C57Bl/6J and AKR/J, were fed regular rodent chow or high-fat diet, after which islet morphology, secretory function and gene expression were assessed. AKR/J had lower blood glucose and higher insulin levels compared with C57Bl/6J mice on regular rodent chow or high fat diet. Insulin secretion was 3.2 fold higher in AKR/J than C57Bl/6J mice following intraperitoneal glucose injection. Likewise, glucose-stimulated insulin secretion from isolated islets was higher in AKR/J. Additionally, islet mass was 1.4 fold greater in AKR/J compared with C57Bl/6J. To elucidate the factors associated with the differences in insulin, we analyzed the gene expression profiles in pancreatic islets in AKR/J and C57Bl/6J mice. Of 14,000 genes examined, 220 were up-regulated and 286 were down-regulated in islets from diet-induced obese AKR/J mice compared with C57Bl/6J mice. Key genes involved in islet signaling and metabolism, e.g. glucagon like peptide-1 receptor, sterol Co-A desaturase 1 & 2 and fatty acid desaturase 2 were upregulated in obese AKR/J mice. The expression of multiple extracellular matrix proteins was also increased in AKR/J mice, suggesting a role in modulation of islet mass. Functional analyses of differentially regulated genes hold promise for elucidating factors linking obesity to alterations in islet function. Keywords: response to high fat diet
2008-02-28 | GSE10639 | GEO
Project description:Background: Acute Respiratory Distress Syndrome (ARDS) or its earlier stage Acute lung injury (ALI), is a worldwide health concern that jeopardizes human well-being. Currently, the treatment strategies to mitigate the incidence and mortality of ARDS are severely restricted. This limitation can be attributed, at least in part, to the substantial variations in immunity observed in individuals with this syndrome. Methods: Bulk and single cell RNA sequencing from ALI mice and single cell RNA sequencing from ARDS patients were analyzed. We utilized the Seurat program package in R and cellmarker 2.0 to cluster and annotate the data. The differential, enrichment, protein interaction, and cell-cell communication analysis were conducted. Results: The mice with ALI caused by pulmonary and extrapulmonary factors demonstrated differential expression including Clec4e, Retnlg, S100a9, Coro1a, and Lars2. We have determined that inflammatory factors have a greater significance in extrapulmonary ALI, while multiple pathways collaborate in the development of pulmonary ALI. Clustering analysis revealed significant heterogeneity in the relative abundance of immune cells in different ALI models. The autocrine action of neutrophils plays a crucial role in pulmonary ALI. Additionally, there was a significant increase in signaling intensity between B cells and M1 macrophages, NKT cells and M1 macrophages in extrapulmonary ALI. The CXCL, CSF3 and MIF, TGFβ signaling pathways play a vital role in pulmonary and extrapulmonary ALI, respectively. Moreover, the analysis of human single-cell revealed DCs signaling to monocytes and neutrophils in COVID-19-related ARDS is stronger compared to sepsis-associated ARDS. In sepsis-associated ARDS, CD8+ T and Th cells exhibit more prominent signaling to B-cell nucleated DCs. Meanwhile, both MIF and CXCL signaling pathways are specific to sepsis-associated ARDS. Conclusions: This study has identified specific gene signatures and signaling pathways in animal models and human samples that facilitate the interaction between immune cells, which could be targeted therapeutically in ARDS patients of various etiologies.
2024-04-24 | GSE264032 | GEO
Project description:Background: Acute Respiratory Distress Syndrome (ARDS) or its earlier stage Acute lung injury (ALI), is a worldwide health concern that jeopardizes human well-being. Currently, the treatment strategies to mitigate the incidence and mortality of ARDS are severely restricted. This limitation can be attributed, at least in part, to the substantial variations in immunity observed in individuals with this syndrome. Methods: Bulk and single cell RNA sequencing from ALI mice and single cell RNA sequencing from ARDS patients were analyzed. We utilized the Seurat program package in R and cellmarker 2.0 to cluster and annotate the data. The differential, enrichment, protein interaction, and cell-cell communication analysis were conducted. Results: The mice with ALI caused by pulmonary and extrapulmonary factors demonstrated differential expression including Clec4e, Retnlg, S100a9, Coro1a, and Lars2. We have determined that inflammatory factors have a greater significance in extrapulmonary ALI, while multiple pathways collaborate in the development of pulmonary ALI. Clustering analysis revealed significant heterogeneity in the relative abundance of immune cells in different ALI models. The autocrine action of neutrophils plays a crucial role in pulmonary ALI. Additionally, there was a significant increase in signaling intensity between B cells and M1 macrophages, NKT cells and M1 macrophages in extrapulmonary ALI. The CXCL, CSF3 and MIF, TGFb signaling pathways play a vital role in pulmonary and extrapulmonary ALI, respectively. Moreover, the analysis of human single-cell revealed DCs signaling to monocytes and neutrophils in COVID-19-associated ARDS is stronger compared to sepsis-related ARDS. In sepsis-related ARDS, CD8+ T and Th cells exhibit more prominent signaling to B cell nucleated DCs. Meanwhile, both MIF and CXCL signaling pathways are specific to sepsis-related ARDS. Conclusion: This study has identified specific gene signatures and signaling pathways in animal models and human samples that facilitate the interaction between immune cells, which could be targeted therapeutically in ARDS patients of various etiologies.
2024-04-17 | GSE263867 | GEO
Project description:Rat model of ARDS was induced by saline lavage and mechanical ventilation. miRNA from rat lungs were used for dual color DNA microarray hybridization with 3DNA 50 kit version 2. Two-condition experiment, CON vs. ARDS lung tissues. replicates: 6 control, 6 ARDS. One replicate per array.
2014-05-07 | E-GEOD-57223 | biostudies-arrayexpress
Project description:Rat model of ARDS was induced by saline lavage and mechanical ventilation. Total RNA from rat lungs were used for dual color DNA microarray hybridization with 3DNA 50 kit version 2. Two-condition experiment, CON vs. ARDS lung tissues. replicates: 5 control, 7 ARDS. One replicate per array.
2014-04-24 | E-GEOD-57011 | biostudies-arrayexpress
Project description:Cryptorchidism and scrotal heating result in abnormal spermatogenesis but the mechanism(s) proscribing this temperature sensitivity are unknown. It was previously reported that the AKR/N or MRL/MpJ-+/+ mouse testis is more heat resistant than the testis from the C57BL/6 strain. We have attempted to probe into the mechanism(s) involved in heat sensitivity by examining global gene expression profiles of normal and heat-treated testes from C57BL/6, AKR/N and MRL/MpJ-+/+ mice by microarray analysis. In the normal C57BL/6 testis, 415 and 416 transcripts were differentially expressed (at least two-fold higher or lower) when compared to the normal AKR/N and MRL/MpJ-+/+ testis, respectively. The AKR/N and MRL/MpJ-+/+ strains revealed 268 differentially expressed transcripts between them. There were 231 transcripts differentially expressed between C57BL/6 and two purported heat-resistant strains, AKR/N and MRL/MpJ-+/+. Next, the testes of C57BL/6 and AKR/N mice were exposed to 43ºC for 15 min and harvested at different time points for TUNEL studies and microarrays. An increase of TUNEL-positive germ cell numbers was significant 8 hr after heat exposure in the C57BL/6 mouse. However, this increase was not observed in the AKR/N mouse until 10 hr after heat exposure. All tubules showed germ cell loss and disruption in C57BL/6 testis 24 hr after heat shock. In contrast, although a number of seminiferous tubules showed an abnormal morphology 24 hr post-heat shock in the AKR/N mouse, many tubules still retained a normal structure. Numerous transcripts exhibited differential regulation between the two strains within 24 hours after heat exposure. The differentially expressed transcripts in the testes 8 hr after heat exposure were targeted to identify the genes involved in the initial response rather than those due to germ cell loss. Twenty transcripts were significantly down-regulated and 19 genes were up-regulated by hyperthermia in C57BL/6 and did not show a parallel change in the AKR/N testis. Conversely, heat shock resulted in 30 up-regulated transcripts and 31 down-regulated transcripts in AKR/N that were not similarly regulated in C57BL/6. A number of genes shared similar differential expression patterns and differential regulation by hyperthermia in both strains of mice. Taken together, the present study indicates the diverse genetic backgrounds in the three strains lead to major differences in normal testis gene expression profiles while the differences in heat shock responses involves a significantly smaller number of genes. The data generated may provide insights regarding gene networks and pathways involved in heat stress and their relationship to spermatogenesis.
2008-11-01 | GSE13010 | GEO