Transcriptomic analysis of primary human umbilical vein endothelial cells (HUVEC). HUVEC were treated in vitro with CoCl2 to induce hypoxia, high glucose and high glucose plus hypoxia in different intervals (1, 3, 12 hours). Subsequently, the effect of metformin (anti-diabetic drug) on all conditions was studied to take advantage of transcriptomics to prospectively explore the mechanism of this drug to reduce the risk of cardiovascular diseases in type II diabetic patients.
Reference genes for expression studies in hypoxia and hyperglycemia models in human umbilical vein endothelial cells.
Specimen part
View SamplesEstrogen-related receptor ? (ERR?) signaling increases during the neonatal to adult transition in pancreatic islet ß-cells. We show that ß-cell-specific ERR?-deficient (ßERR?KO) mice exhibit glucose intolerance with reduced glucose-stimulated insulin secretion (GSIS) and ßERR?KO islets have defective GSIS function accompanied by changes in genes that regulate ATP biosynthesis, oxidative phosphorylation, and the electron transport chain. ERR? overexpression enhances genes involved in mitochondrial metabolism, resulting in transformation of ß-like-cells into metabolically functional ß-cells that can ameliorate STZ-induced hyperglycemia in NOD-SCID mice. These results suggest that ERR? signaling is essential for the metabolic maturation of ß-like-cells and thus represents a novel therapeutic target in the treatment of diabetes.
ERRγ Is Required for the Metabolic Maturation of Therapeutically Functional Glucose-Responsive β Cells.
No sample metadata fields
View SamplesWe characterized the effect of loss of ERR expression in mouse pancreatic islets using adenoviral constructs.
ERRγ Is Required for the Metabolic Maturation of Therapeutically Functional Glucose-Responsive β Cells.
Specimen part
View SamplesWe show that ERR? overexpression in ß-like-cells differentiated from human iPSCs enhances genes involved in mitochondrial metabolism, resulting in transformation of these cells into metabolically functional ß-cells that can ameliorate STZ-induced hyperglycemia in NOD-SCID mice. These results suggest that ERR? signaling is essential for the metabolic maturation of ß-like-cells and thus represents a novel therapeutic target in the treatment of diabetes.
ERRγ Is Required for the Metabolic Maturation of Therapeutically Functional Glucose-Responsive β Cells.
No sample metadata fields
View SamplesTranscriptomic analysis of primary CD34+ cells. CD34+ cell were induced in vitro with hypoxia (3 hours), high glucose and high glucose plus hypoxia. Subsequently, the effect of metformin (anti-diabetic drug) on all conditions was studied to take advantage of transcriptomics to prospectively explore the mechanism of this drug to reduce the risk of cardiovascular diseases in type II diabetic patients.
Metformin improves the angiogenic potential of human CD34⁺ cells co-incident with downregulating CXCL10 and TIMP1 gene expression and increasing VEGFA under hyperglycemia and hypoxia within a therapeutic window for myocardial infarction.
Specimen part
View SamplesWe performed RNA sequencing analysis of hepatic gene expression a few hours after amlexanox treatment, and identified over 1700 differentially expressed genes. Pathway analysis of these differentially regulated genes revealed that the top two most enriched pathways were the adipocytokine signaling pathway and the Jak-STAT signaling pathway. Overall design: RNA-seq analysis of hepatic gene expression was used to identify differentially expressed genes in response to Amlexanox treatment.
A subcutaneous adipose tissue-liver signalling axis controls hepatic gluconeogenesis.
No sample metadata fields
View SamplesPurpose: The goals of this study are to determine the effect of microRNA-17 overexpression on 20,803 human genes in RASFs using Ion ProtonTM System platform. Human RASFs from two RA patients were transfected with pre-miR-17 or NC-pre-miR for 48 h and total RNA was prepared using miRNeasy kit (Qiagen). Total RNA integrity was checked using an Agilent Technologies 2100 Bio analyzer (Santa Clara, CA). 10 ng of high quality RNA was used to make cDNA for amplification with the Ion AmpliSeq Transcriptome Human Gene Expression kit (ThermoFisher Scientific). The cDNA was subjected to 12 cycles of amplification with panel primers and barcoded with adapters as recommended. Resulting sequencing libraries were quantified by qPCR using SYBR FAST master mix from KapaBiosystems (Wilmington, MA). Sets of eight libraries were balanced, pooled and sequencing beads produced on an Ion Chef. Sequencing was performed on an Ion P1 semi-conductor sequencing chip using an Ion Proton™ System (ThermoFisher Scientific, Grand Island, NY). Data was collected and primary analysis performed using Torrent Suite software version 5.0.3. Reads were mapped to the panel and expression values determined. R Software version R-3.2.3 was used to generate heatmap. Among the panel of 20,803 genes, the expression of 15,067 genes as shown in the representative heat map was observed in pre-miR-17 and NC-pre-miR transfected RASFs. A total of 664 significantly modulated genes (301 upregulated and 363 downregulated) using Student ‘t’ test were further utilized for the IPA analysis. The result of IPA predicted the protein ubiquitin pathway as a major canonical pathway affected by the differentially regulated genes. Interestingly, IPA analysis generated an interactome that showed connectivity among various ubiquitin ligases, NF-?B family, AP-1/cJun, 20S and 26S proteasome system. Conclusion: Our results clearly shows the major pathways affected by miR-17 overexpression in RASFs were Protein ubiquitination related. Overall design: mRNA profiles of pre-miR-17 and NC-pre-miR transfected RASFs were generated by AmpliSeq, in duplicate, using Ion Proton™ System.
MicroRNA-17 Suppresses TNF-α Signaling by Interfering with TRAF2 and cIAP2 Association in Rheumatoid Arthritis Synovial Fibroblasts.
Specimen part, Subject
View SamplesIndividuals expressing alpha-1-antitrypsin mutant Z protein accumulate misfolded, mutant protein in the liver and are at risk for liver diseases including cirrhosis and hepatocellular carcinoma. Transgenic PiZ mice, a model for this liver disease, display similar pathologies to humans, including inflammation, increases in proliferation, autophagy and apoptosis, accumulation of globules and develop fibrosis and hepatocellular carcinoma with age. Microarrays were used to compare the gene expressions of PiZ mice to wild-type mice in order to identify the pathways that are altered in this disorder.
Oxidative stress contributes to liver damage in a murine model of alpha-1-antitrypsin deficiency.
Sex, Specimen part
View SamplesExpression profiling of isoflavone and 3,3-diindolylmethane treated C4-2B prostate cancer cells was conducted using Affymetrix Human Genome U133 Plus 2.0. Array
Targeting bone remodeling by isoflavone and 3,3'-diindolylmethane in the context of prostate cancer bone metastasis.
Cell line, Time
View SamplesSummary: Brain trauma is a major cause of morbidity and mortality, both in adult and pediatric populations. Much of the functional deficit derives from delayed cell death resulting from induction of neurotoxic factors that overwhelm endogenous neuroprotective responses.
Gene expression profile changes are commonly modulated across models and species after traumatic brain injury.
No sample metadata fields
View Samples