17beta-hydroxysteroid dehydrogenase type12 (HSD17B12) has been demonstrated to be involved in regulation of in situ biosynthesis of estradiol (E2). HSD17B12 expression was reported in breast carcinomas but its functions have remained unknown. Therefore, we examined the correlation between mRNA expression profiles determined by microarray analysis and tissue E2 concentrations obtained from 16 postmenopausal breast carcinoma cases in order to analyze an association of the enzyme expression with intratumoral E2 production. No significant correlations were detected between intratumoral HSD17B12expression and E2 concentration.These findings suggest that the presence of HSD17B12 in carcinoma cells contributes to a development of human breast carcinoma via a pathway other than in situ E2 biosynthesis.
17Beta-hydroxysteroid dehydrogenase type 12 in human breast carcinoma: a prognostic factor via potential regulation of fatty acid synthesis.
Sex, Specimen part
View SamplesTo examine irreversible changes in the developing brain following seizures, juvenile inbred mice were intraperitoneally injected with kainate and nicotine.
Increased expression of the lysosomal protease cathepsin S in hippocampal microglia following kainate-induced seizures.
No sample metadata fields
View SamplesIdiopathic portal hypertension (IPH) is characterized by portal hypertension due to obstruction or stenosis of the intrahepatic peripheral portal branches. Researchers have suggested that IPH may be attributed to intrahepatic peripheral portal vein thrombosis, splenic factors, abnormal autoimmunity, and related factors, however, the etiology of IPH remains unclear.
Comprehensive Screening of Gene Function and Networks by DNA Microarray Analysis in Japanese Patients with Idiopathic Portal Hypertension.
Specimen part, Disease stage
View SamplesAge-dependent electrical and morphological remodeling of the Drosophila heart caused by hERG/seizure mutations
Age-dependent electrical and morphological remodeling of the Drosophila heart caused by hERG/seizure mutations.
No sample metadata fields
View SamplesAltered gene expression in the sphingosine 1-phosphate receptor 2 (S1P2)-deficient or sphingosine 1-phosphate receptor 3 (S1P3)-deficient brain.
Frequent spontaneous seizures followed by spatial working memory/anxiety deficits in mice lacking sphingosine 1-phosphate receptor 2.
No sample metadata fields
View SamplesCellular differentiation is regulated through activation and repression of defined transcription factors. A hallmark of differentiation is a pronounced change in cell shape, which is determined by dynamics of the actin cytoskeleton. In de-differentiated fat (DFAT) cells and 3T3-L1 cells, we showed that treatment with the ROCK inhibitor Y-27632, by inducing remodeling of the actin cytoskelton, causes adipocyte differentiation. In addition, we found that depletion of MKL1, an actin binding transcriptional coactivator, elicits adipogenesis.
Regulation of MKL1 via actin cytoskeleton dynamics drives adipocyte differentiation.
Specimen part
View SamplesProliferative diabetic retinopathy (PDR) is a vision-threatening disorder characterized by the formation of cicatricial fibrovascular membranes leading to traction retinal detachment. Despite the recent advance in the treatment of PDR such as vitreoretinal surgery with use of anti-vascular endothelial growth factor (VEGF) drug as an adjunct, it still remains vision-threatening disease.
Microarray analysis of gene expression in fibrovascular membranes excised from patients with proliferative diabetic retinopathy.
Specimen part, Disease, Disease stage
View SamplesSome neuropsychiatric disease, including schizophrenia, may originate during prenatal development, following periods of gestational hypoxia and placental oxidative stress. Here we investigated if gestational hypoxia promotes damaging secretions from the placenta that affect fetal development and whether a mitochondria-targeted antioxidant MitoQ might prevent this. Gestational hypoxia caused low birth-weight and changes in young adult offspring brain, mimicking those in human neuropsychiatric disease. Exposure of cultured neurons to fetal plasma or to secretions from the placenta or from model trophoblast barriers that had been exposed to altered oxygenation caused similar morphological changes. The secretions and plasma contained altered microRNAs whose targets were linked with changes in gene expression in the fetal brain and with human schizophrenia loci. Molecular and morphological changes in vivo and in vitro were prevented by a single dose of MitoQ bound to nanoparticles, which were shown to localise and prevent oxidative stress in the placenta but not in the fetus. We suggest the possibility of developing preventative treatments that target the placenta and not the fetus to reduce risk of psychiatric disease in later life. Overall design: 16 samples (4 biological replicates per group) were analysed using RNA sequencing. The 4 groups were: Normoxia+Saline (control sample), Normoxia+MitoQ-NP, Hypoxia+Saline and Hypoxia+MitoQ-NPs. Pair-wise comparison between all groups was performed.
Treating the placenta to prevent adverse effects of gestational hypoxia on fetal brain development.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
PU.1 is a potent tumor suppressor in classical Hodgkin lymphoma cells.
Cell line, Time
View SamplesPU.1 is an Ets family transcription factor that is essential for the differentiation of both myeloid and lymphoid cells. PU.1 is down-regulated in classical Hodgkin lymphoma cells via methylation of the PU.1 promoter. To evaluate whether down-regulation of PU.1 is essential for the growth of cHL cells, we generated KM-H2 derived cell lines conditionally express PU.1 by tet-off system (designated KM-H2tetPU.1). Conditonally expressed PU.1 by tetracycline removal induced complete growth arrest and apoptosis in KM-H2 cells. To elucidate the mechanisms underlying cell cycle arrest and apoptosis induced by PU.1, we compared gene expression profiles of KM-H2tetPU.1 cells 0, 1 and 3 days after PU.1 induction, by DNA microarray.
PU.1 is a potent tumor suppressor in classical Hodgkin lymphoma cells.
Cell line, Time
View Samples