A goal of this study was to identify and investigate previously unrecognized components of the remodeling process in the progression to heart failure by comparing gene expression in ischemic, failing (F) to non-failing (NF) hearts. These results also were compared to the changes observed in a proteomic analysis of F and NF hearts.
Differential protein expression and basal lamina remodeling in human heart failure.
Specimen part
View SamplesFour male SHR/Ola, BN and SHR-18 rats were fed a normal diet and sacrificed at 9 weeks of age. Four male SHR/Ola and SHR-18 rats at 8 weeks of age were fed 1% NaCl for one week and then sacrificed. Kidneys were removed and frozen in liquid nitrogen for all 20 animals. Total RNA was isolated, labelled cRNA was generated and hybridised to Affymetrix Rat RG-U34ABC arrays.
Dissection of chromosome 18 blood pressure and salt-sensitivity quantitative trait loci in the spontaneously hypertensive rat.
Sex, Age, Specimen part
View SamplesRight ventricular failure was induced thourgh pulmonary banding in 11 pigs. Right ventricular failure was defined as a SRVP >50 mmHg during two hours. After right ventricular failure was induced, half the pigs were treated with a Glenn-shunt combined with pulmonary banding for one hour, and the other half served as control group with pulmonary banding only. The aim was to study the change in global gene expression during right ventricular failure due to pulmonary banding, and the effect of volume unloading during pulmonary banding.
A modified Glenn shunt reduces venous congestion during acute right ventricular failure due to pulmonary banding: a randomized experimental study.
Specimen part, Treatment
View SamplesIn this study, we use pre-malignant cells from different Cebpa mutant acute myeloid leukemia (AML) models. We have used conditional KO models (CreLoxP) and isolated hematopoietic cells shortly after induction of recombination, in order to look at pre-leukemic cells, which have acquired the first hit, but not yet undergone full malignant transformation.
Lack of the p42 form of C/EBPα leads to spontaneous immortalization and lineage infidelity of committed myeloid progenitors.
Sex, Specimen part
View SamplesTo identify factors and pathways regulated by IMP proteins and obtain leads to the mechanism behind the phenotypic changes, we compared the gene expression profiles of IMP siRNA treated cells with mock treated cells. Triplicate gene expression profiles were generated from both the IMP(1,3)A and IMP(1,3)B siRNA sets and were compared to the mock transfected cells. cRNA was hybridized to Affymetrix human U133A arrays.
RNA-binding IMPs promote cell adhesion and invadopodia formation.
Specimen part, Cell line
View SamplesWe recently isolated and identified (7E)-9-oxohexadec-7-enoic acid (1) and (10E)-9-oxohexadec-10-enoic acid (2) from the marine algae Chaetoceros karianus. Synthesis and biological characterization show that these are PPARa/? dual agonists. Herein we report the gene expression data from human SGBS pre-adipocytes, stimulated to differentiate with 1, 2 or the classical PPAR? agonist rosiglitazone. The transcriptome analysis shows that both compounds induce anti-diabetic gene programs in adipocytes by upregulating insulin-sensitizing adipokines and repressing pro-inflammatory cytokines. Overall design: Human SGBS pre-adipocytes were stimulated with adipogenic media supplemented with either (7E)-9-oxohexadec-7-enoic acid, (10E)-9-oxohexadec-10-enoic acid, or rosiglitazone from day 0 to day 4. On day 4, agonists were withdrawn, and the cells were allowed to differentiate following standard protocol. On day 8, RNA was isolated and sent to sequencing.
Synthesis and biological evaluations of marine oxohexadecenoic acids: PPARα/γ dual agonism and anti-diabetic target gene effects.
Specimen part, Cell line, Subject
View SamplesThe anaphylatoxin C5a is a potent mediator of innate immunity and promotes inflammation via its receptor C5aR1 upon complement system activation danger-associated molecular patterns. Both C5a and C5aR1 are thought to be contributing factors in inflammatory and infectious conditions of the bone. Bone fracture healing, for example, was significantly improved when applying a C5aR1-antagonist in a rodent model of severe systemic inflammation and osteoblasts were found to be target cells for C5a in this setting. Interestingly, osteoblasts up-regulate C5aR1 during osteogenic differentiation and after bone injury. Further, C5a induces inflammatory cytokines, such as IL-6, and the osteoclastogenic mediator RANKL in osteoblasts. However, the molecular mechanisms underlying C5a-C5aR1 signaling axis in osteoblasts remain unclear, and further targets of C5a are still elusive. Using microarray analysis, we analyzed intracellular events following C5aR1 activation in osteoblasts and defined up- or down-regulated genes and their belonging biological pathways.
C5aR1 interacts with TLR2 in osteoblasts and stimulates the osteoclast-inducing chemokine CXCL10.
Treatment
View SamplesThe aim of the study was to identify candidate genes responsible for drought tolerance trait between a pair of wheat varieties ( WL711 and C306) and correspondng progeny bulks (10 drought susceptible RILs and 10 drought tolerant RILs) by combining QTLs analysis with expression analysis. Microarray analysis of RNA extracted from the flag leaves showed large number of differentially expressed genes. The number of differentially expressed genes was reduced to 37 on the basis of their occurance in a major QTL region (responcible for drought tolerance) detected in RIL population derived from WL711 and C306.
Genomic associations for drought tolerance on the short arm of wheat chromosome 4B.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Knockdown of NAT12/NAA30 reduces tumorigenic features of glioblastoma-initiating cells.
Specimen part, Treatment
View SamplesGene knockdown of NAT12/NAA30 led to decreased proliferation, sphere forming ability and mitochondrial hypoxia tolerance in the GSC T65 culture. Intracranial transplantation of these cells into SCID mice showed that the decreased NAT12/NAA30 expression correlated with the prolonged animal survival and reduced tumor size
Knockdown of NAT12/NAA30 reduces tumorigenic features of glioblastoma-initiating cells.
Specimen part, Treatment
View Samples