Adipose tissue RNAseq in T-cell-specific IFNAR-deficient mice.
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE118819 | GEO | 2019/05/31
REPOSITORIES: GEO
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Project description:Adipose tissue RNAseq in T-cell-specific IFNAR-deficient mice.
| PRJNA486902 | ENA
Project description:Purpose: While type I interferons (IFN) are important for control of viral replication, we see that, upon infection of Ifnar-/- females were crossed to Ifnar+/- males with ZIKV, only Ifnar+/- fetuses are resorbed or develop severe growth restriction. To identify how IFN may be altering placenta development, we performed RNAsequencing on infected and uninfected Ifnar-/- and Ifnar+/- placentas. Methods: Ifnar-/- females were crossed to Ifnar+/- males and infected intravaginally with Cambodian ZIKV at E5.5. Placentas were harvested from infected and uninfected pregnant dams at E10.5. Results/ Conclusions: Comparison of ZIKV-infected Ifnar-/- and Ifnar+/- shows an elevated interferon stimulated gene (ISG) signature in Ifnar+/- placentas but does not reveal any underlying developmental defects that may be causing defects in placenta development.
2017-12-31 | GSE98423 | GEO
Project description:The regulatory gene pathways underlying the loss of adipose tissue in cancer cachexia are unknown and were explored using pangenomic transcriptome profiling. Gene expression profiles (Human Gene 1.0 ST) of abdominal subcutaneous adipose tissue were studied in gastrointestinal cancer patients with (N=13) or without (N=14) cachexia. Data analyses were performed using the Affymetrix GeneChip Operating Software (GCOS) Version 1.4.
2010-04-10 | E-GEOD-20571 | biostudies-arrayexpress
Project description:Cancer-associated cachexia (CAC) is a wasting syndrome caused by malignant tumors. Fat loss plays a significant role in the pathophysiology of cancer-associated cachexia. The mechanism of fat loss in CAC includes enhancement of lipolysis, inhibition of lipogenesis and browning of white adipose tissue. In order to discover potentially functional genes in white adipose tissue of CAC, we used transcriptome sequencing technology to find research-valuable genes in white adipose tissue (WAT) of CAC rodent model. C57/bl6 mice with LLC tumors were used as the in vivo model for CAC, while normal mice subcutaneously injected with phosphate buffer solution were used as the control group. Overall, our data revealed genes that were differentially expressed in the white adipose tissue of LLC tumor-bearing mice, providing a molecular framework for the investigation into CAC fat loss.
2023-09-15 | GSE242812 | GEO
Project description:Cancer cachexia is a severe systemic wasting disease that negatively affects quality of life and survival in patients with cancer. To date, treating cancer cachexia is still a major unmet clinical need. We recently discovered the destabilization of the AMPK complex in adipose tissue as a key event in cachexia-related adipose tissue dysfunction and developed an AAV-based approach to prevent AMPK degradation and prolong cachexia-free survival. Here, we show the development and optimization of a prototypic peptide, Pen-X-ACIP, where the AMPK stabilizing peptide ACIP is fused to the cell-penetrating peptide moiety penetratin via a propargylic glycine linker to enable late-stage functionalization using click chemistry. Pen-X-ACIP was efficiently taken up by adipocytes, inhibited lipolysis and restored AMPK signaling. Tissue uptake assays showed a favorable uptake profile into adipose tissue upon intraperitoneal injection. Systemic delivery of Pen-X-ACIP into tumor-bearing animals prevented the progression of cancer cachexia without affecting tumor growth, and preserved body weight and adipose tissue mass with no discernable side effects in other peripheral organs, thereby achieving proof-of-concept. As Pen-X-ACIP also exerted its anti-lipolytic activity in human adipocytes, it now provides a promising platform for further (pre)clinical development towards a novel, first-in-class approach against cancer cachexia.
2023-07-02 | GSE235940 | GEO
Project description:The regulatory gene pathways underlying the loss of adipose tissue in cancer cachexia are unknown and were explored using pangenomic transcriptome profiling.
2010-04-10 | GSE20571 | GEO
Project description:Cancer-associated cachexia (CAC) is a metabolic syndrome characterized by progressive depletion of adipose and muscle tissue which cannot be corrected by conventional nutritional therapy. Adipose tissue, as an important energy storage, could appear obvious loss in early stage of CAC, which becomes a negative factor affecting the quality of life, efficacy of chemotherapy and so on. In order to identify differentially expressed RNAs in adipose tissue of CAC patients with noncachexia patients, we chose three gastric cancer patients with remarkable weight loss as CAC group and three gastric cancer patients without significant weight change within half a year as the control group. We resected a small subcutaneous adipose tissue from the abdomen of these six patients at time of surgery and completed transcriptome sequencing using Illumina platform. Compared with NCBI genome detabase, etc, we finally identified 386 differentially expressed mRNAs, 410 differentially expressed lncRNAs, 66 differentially expressed cirRNAs and 98 differentially expressed miRNAs. We hoped to provide more bases for follow-up study of adipose metabolism in cachexia.
2021-05-10 | GSE174128 | GEO
Project description:Pancreatic ductal adenocarcinoma (PDAC) causes involuntary wasting of adipose and muscle tissue, also known as cachexia. Cachexia is a major cause of cancer-related deaths, particularly among patients with PDAC. Here we profiled gene expression in adipose tissue and skeletal muscle in normal/sham control mice and in mice bearing orthotopic PDAC tumors. PDAC tumors were initiated by intra-pancreatic injection of a cell line derived from the KPC (Kras-G12D;Trp-R172H;Pdx1::Cre) genetically engineered mouse model of pancreatic cancer, or by injection of the same cell line deleted for the IL6 gene using CRISPR/Cas9. KPC-IL6 knockout (ko) cells caused less adipose wasting and no muscle loss compared with KPC-wildtype (wt) cells.
2021-04-07 | GSE123310 | GEO
Project description:Endothelial cells form a barrier between the contents of the blood and adipocytes. We hypothesized that during cancer cachexia development, transcriptomic changes alter angiocrine signals to contribute to adipose tissue remodelling. We used microarrays to observe changes in gene expression in endothelial cells isolated from subcutaneous fat of mice during pre-cachexia.
2023-06-19 | GSE212562 | GEO
Project description:Purpose: Cachexia is a metabolic phenotype affecting many cancer patients. The immune environment in adipose tissue during the development of cancer associated cachexia has not been characterized. To help address this gap, we isolated visceral adipose tissue from cancer-bearing and sham-operated mice and performed bulk RNA-sequencing. Methods: mRNA expression was evaluated by RNA-sequencing in visceral adipose tissue (VAT) of 10-week old mice which had been subjected to sham surgery (sham) or had received orthotopic pancreatic tumors four weeks prior to harvest (KPC). Paired-end 150 bp single-index sequencing was performed using an Illumina HiSeq system. Transcript quantification was performed with Salmon, using quasi-mapping mode with selective alignment (validateMappings). We set the rangeFactorizationBins to 4 and passed both the seqBias and gcBias flags to correct for sequence-specific bias and fragment-level GC bias, respectively. Transcript quantifications were collapsed to gene-level quantifications using the tximport package and the Ensembl based annotation package EnsDb.Mmusculus.v79. Differential expression analysis was then performed using DESeq2 with fold change shrinkage by ashr. For downstream analysis and visualization, only genes with a mean TPM (transcripts per million) > 2 in VAT from both sham-operated and tumor-bearing mice were considered. Results: We identified over 11,000 genes which were expressed at an average of at least 2 TPM (transcripts per million) in both the sham and KPC adipose tissue samples. Differential expression analysis with DESeq revealed 161 upregulated genes (p < 0.05) and 27 downregulated genes (p < 0.05) in the adipose tissue of cancer bearing mice compared to that of sham operated mice. Gene set enrichment analysis suggested an increase in inflammatory pathways, including type 1 and type 2 interferon pathways, in the adipose tissue of cancer bearing mice. Conclusions: This study represents a comprehensive characterization of adipose tissue in the healthy vs. cachexia setting. The RNA-seq data suggests increased immune infiltration into adipose tissue in the setting of a distant pancreatic tumor. Together with flow cytometry and cytokine abundance analyses, we conclude that reguatory Th2 immunity is maintained in the adipose tissue during this model of cancer associated cachexia.
2021-04-03 | GSE171402 | GEO