Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA295984 | ENA |
REPOSITORIES: ENA
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Project description:Amyloidogenic peptides are therapeutic in EAE, reducing systemic levels of IL6, TNF, and INFg. The fibrils are bound and endocytosed in peritoneal MFs and B1a cells. Differential gene expression was used to further understand the process. Groups of three female C57BL/6 mice were injected with 10ug of Tau 623-628, Amylin 28-33, LPS, or PBS. 30-40 minutes post injection, the peritoneal cavity was lavaged, CD11b high (MFs) and CD5+CD19+ (B1a lymphocytes) were purified by flow cytometry directly into Trizol. RNA was extracted from the aqueous phase using the Qiagen RNeasy microkits. RNA quality was assessed using the Agilent 2100 bioanalyzer and the RNA 6000 nano reagents kit. One color microarray, Agilent-028005 SurePrint G3 Mouse GE 8x60K Microarray, was performed at the human immune monitoring center. All samples were processed and run at the same time.
2015-09-15 | E-GEOD-73026 | biostudies-arrayexpress
Project description:Amyloidogenic peptides are therapeutic in EAE, reducing systemic levels of IL6, TNF, and INFg. The fibrils are bound and endocytosed in peritoneal MFs and B1a cells. Differential gene expression was used to further understand the process.
2015-09-15 | GSE73026 | GEO
Project description:There is a need for greater understanding of the molecular mechanism underlying the development of insulin resistance in type 2 diabetes, and new models in which to study this. The hormone amylin is postulated to be involved in the development of this disease, as human amylin (hA) forms amyloid in the pancreases of diabetic patients, and wild-type hA oligomers have been shown to be cytotoxic to β-cells. By contrast, rodent amylin is non-amyloidogenic, so mice expressing wild-type hA have been developed. However, amylin-evoked β-cell loss in these models limits the secretion of amylin and insulin. We have developed transgenic mice that overexpress [25, 28, 29triprolyl]human amylin, a non-amyloidogenic variant of amylin, designated the Line 44 (L44) model. These mice develop obesity and hyperglycaemia. We examined the expression of 43 genes involved in amylin, insulin and leptin signalling in the brain of this model, at different disease stages, using the NanoString nCounter (NanoString Technologies, Seattle, WA, USA). After onset of diabetes, mice remained hyperglycaemic for a period of time but blood glucose levels eventually returned to normoglycaemia. The incidence of diabetes (defined as having blood glucose measurements > 11 mM over 3 consecutive weeks) was gene-dose dependent; 81% of homozygous mice and 59% of hemizygous mice developed diabetes over 400 days. A proportion of nontransgenic mice (33%) also developed diabetes. As these were bred from hemizygous pairs this may be the result of epigenetic or environmental factors.
2019-10-10 | GSE132940 | GEO
Project description:Mouse peritoneal B1a cells were classified into two groups based upon the expression level of PC1. One is PC1 high group and the other is PC1 low. To evaluate gene expression patterns that distinguished PC1 high expressing B1a cells from PC1 low expressing B1a cells, we used Affymetrix GeneChip® Mouse gene 1.0 ST Array.
2012-07-09 | GSE39171 | GEO
Project description:Mouse peritoneal B1a cells were classified into two groups based upon the expression level of PC1. One is PC1 high group and the other is PC1 low. To evaluate gene expression patterns that distinguished PC1 high expressing B1a cells from PC1 low expressing B1a cells, we used Affymetrix GeneChipM-BM-. Mouse gene 1.0 ST Array. FACS-sorted PC1 high and low cells from individual mouse were used for RNA extraction and Affyarray hybridization. There were six independent biological replications in each group - six cases of PC1 high cells and six cases of PC1 low cells.
2012-07-08 | E-GEOD-39171 | biostudies-arrayexpress
Project description:Sle2c1 is an NZM2410-derived lupus susceptibility locus that induces an expansion of the B1a cell compartment. B1a cells have a repertoire enriched for autoreactivity, and an expansion of this B cell subset occurs in several mouse models of lupus. Here we showed that expression of Sle2c1 enhances NZB cellular phenotypes that have been associated with autoimmune pathogenesis. A combination of genetic mapping and candidate gene analysis presents Cdkn2c, a gene encoding for cyclin kinase inhibitor p18INK4c (p18), as the top candidate gene for inducing the Slec2c1 associated expansion of B1a cells. A novel SNP in the Cdkn2c promoter is associated with a significantly reduced Cdkn2c expression in the splenic B cells and B1a cells from Sle2c1-carrying mice, which leads to defective G1 cell cycle arrest in splenic B cells and increased proliferation of Pc B1a cells. As cell cycle is differentially regulated in B1a and B2 cells, these results suggest that Cdkn2c play a critical role in B1a cell self renewal, and that its impaired expression leads to an accumulation of these cells with high autoreactive potential. Total RNA from peritoneal cavity B cells (B1a) and splenic B cells (Bs) was isolated, with 4 biological replicates each. Gene expression data from C57BL/6 mice were compared with data from B6.Sle2c1 mice.
2010-07-24 | E-GEOD-23114 | biostudies-arrayexpress
Project description:The purpose of this experiment was to determine changes in gene expression by bone marrow-derived macrophages (BMDMs) treated with synthetic human vs. rodent islet amyloid polypeptide (IAPP). Synthetic human IAPP at 15 uM aggregates to form fibrils in vitro, whereas rodent IAPP is non-amyloidogenic. We hypothesized that interaction of macrophages with human IAPP aggregates can activate pro-inflammatory signalling pathways in macrophages, as described for other amyloidogenic peptides.
2010-08-11 | GSE23534 | GEO
Project description:Recent research has shown that peripheral treatment with amylin reduces Alzheimer’s disease (AD) pathology in the brain and improves learning and memory in AD mouse models. To understand the mechanism underlying this novel treatment for AD, we interrogated the transcriptome for changes in cortical gene expression in amyloid precursor protein (APP) transgenic mice treated with amylin compared to a vehicle treated group and wild type (WT) mice. Using weighted gene co-expression network analysis, we discovered that amylin treatment influenced two gene modules linked to AD pathology: 1) a module related to proinflammation and transport/vesicle process that included a hub gene of Cd68, and 2) a module related to mitochondria function that included a hub gene of Atp5b. Amylin treatment restored the expression of most genes in the APP cortex toward levels observed in the WT cortex including 23 key hub genes in these two modules. In cultured activated microglia cell line BV-2, we validated that Cd68 expression was attenuated by amylin through binding to the amylin receptor. Using publically-available transcriptomic human data, we found that the expression levels of the orthologues of these hub genes, including Cd68 and Atp5b, strongly correlated with the neurofibrillary tangle burden in the AD brain and with Mini-Mental Status Exam scores. Our study is the first to show the transcriptome-wide targets of amylin treatment, and further supports the potential use of amylin-type peptides to treat AD.
2017-02-01 | GSE77373 | GEO
Project description:The purpose of this experiment was to determine changes in gene expression by bone marrow-derived macrophages (BMDMs) treated with synthetic human vs. rodent islet amyloid polypeptide (IAPP). Synthetic human IAPP at 15 uM aggregates to form fibrils in vitro, whereas rodent IAPP is non-amyloidogenic. We hypothesized that interaction of macrophages with human IAPP aggregates can activate pro-inflammatory signalling pathways in macrophages, as described for other amyloidogenic peptides. This array includes eight samples from one experiment, with two groups of four replicates each. Each replicate represents BMDMs from one well of a 24-well plate. The control group was treated with 15 uM rat IAPP for 12 hours prior to total RNA extraction; the experimental group was treated with 15 uM human IAPP.
2010-08-11 | E-GEOD-23534 | biostudies-arrayexpress
Project description:Peritoneal metastasis (PM) has a suppressive tumor immune microenvironment (TIME), which limits the effects of immunotherapy. This study aims to investigate the immunomodulatory effects of intraperitoneal administration of IL-33 on PM-associated TIME. Immunocompetent mice were used to investigate the role of IL-33 in development of abdominal dissemination and host outcome. Murine (m) and human (h) gastric cancer cells were tested for their response to IL-33 by qRT-PCR, flow cytometry, and immunofluorescence. Survival was significantly prolonged in patients with high Il-33 mRNA expression. Intraperitoneal administration of IL-33 could induce the celiac inflammatory environment, activate immunologic effector cells and reverse the immunosuppressive tumor microenvironment, which delayed tumor progression and peritoneal metastasis of gastric cancer. Mechanistically, IL-33 could induce M2 polarization by activating p38-GATA-binding protein 3 (GATA3) signaling pathway. IL-33 combined with anti-CSF1R or p38 inhibitor to regulate tumor-associated macrophages (TAMs) showed synergistic anti-tumor effect. Intraperitoneal administration of IL-33 inducing local inflammatory milieu provided a novel approach for the treatment of metastatic peritoneal malignancies, which combined with TAMs reprogramming to reshape TIME could achieve better treatment efficacy.
2023-06-30 | GSE235526 | GEO