Middle cerebral artery occlusion (MCAo) in rat represent the ischemic stroke in human. Rodents subjected to MCAo and treated with venom phospholipase A2 showed reduction in infarct volume after 24hours of stroke.
A secretory phospholipase A2-mediated neuroprotection and anti-apoptosis.
No sample metadata fields
View SamplesThe molecular responses of Grey poplar (Populus x canescens) following root hypoxia were studied in roots and leaves using transcript profiling. Grey poplar is a flooding tolerant tree species and analysis of the molecular response to hypoxia may indicate possible adaptation mechanisms to this stress.
Differential response of gray poplar leaves and roots underpins stress adaptation during hypoxia.
No sample metadata fields
View SamplesLaser capture microdissection was used to obtain individual LGN layers for DNA microarray of Rhesus array in macaque monkeys that Monocular Visual Deprivation was generated by either opaque dark contact lens or tarsoraphoplasty at birth.
Monocular visual deprivation in macaque monkeys: a profile in the gene expression of lateral geniculate nucleus by laser capture microdissection.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Epithelial and stromal microRNA signatures of columnar cell hyperplasia linking Let-7c to precancerous and cancerous breast cancer cell proliferation.
Sex, Specimen part, Disease, Disease stage, Treatment
View SamplesPulmonary hypoxia is a common complication of chronic lung diseases leading to the development of pulmonary hypertension. The underlying sustained increase in vascular resistance in hypoxia is a response unique to the lung. Thus, we hypothesised that there are genes whose expression is altered selectively in the lung in response to alveolar hypoxia.
Lung-selective gene responses to alveolar hypoxia: potential role for the bone morphogenetic antagonist gremlin in pulmonary hypertension.
No sample metadata fields
View SamplesColumnar cell hyperplasia (CCH) is the first histologically identifiable lesion in the breast with premalignant potential. Altered miRNA expression in the stroma surrounding CCH compared to normal tissue was discovered. The effect of upregulation of one specific miRNA was investigated by gene expression array in human mammary fibroblasts as well as in epithelial CCH cells coculterd with miR-132 oversexpressing human mammary fibroblasts.
Epithelial and stromal microRNA signatures of columnar cell hyperplasia linking Let-7c to precancerous and cancerous breast cancer cell proliferation.
Specimen part, Treatment
View SamplesHistone deacetylase 9 (HDAC9) is expressed in B cells, and its overexpression has been observed in B-lymphoproliferative disorders, including B-cell non-Hodgkin lymphoma (B-NHL). We examined HDAC9 protein expression and copy number alterations in primary B-NHL samples, identifying high HDAC9 expression among various lymphoma entities and HDAC9 copy number gains in 50% of diffuse large B-cell lymphoma (DLBCL). To study the role of HDAC9 in lymphomagenesis, we generated a genetically engineered mouse (GEM) model that constitutively expressed an HDAC9 transgene throughout B-cell development under the control of the immunoglobulin heavy chain (IgH) enhancer (E). Here, we report that the E-HDAC9 GEM model develops splenic marginal zone lymphoma and lymphoproliferative disease (LPD) with progression towards aggressive DLBCL, with gene expression profiling supporting a germinal center cell origin, as is also seen in human B-NHL tumors. Analysis of E-HDAC9 tumors suggested that HDAC9 might contribute to lymphomagenesis by altering pathways involved in growth and survival, as well as modulating BCL6 activity and p53 tumor suppressor function. Epigenetic modifications play an important role in the germinal center response, and deregulation of the B-cell epigenome as a consequence of mutations and other genomic aberrations are being increasingly recognized as important steps in the pathogenesis of a variety of B-cell lymphomas. A thorough mechanistic understanding of these alterations will inform the use of targeted therapies for these malignancies. These findings strongly suggest a role for HDAC9 in B-NHL and establish a novel GEM model for the study of lymphomagenesis and, potentially, preclinical testing of therapeutic approaches based on histone deacetylase inhibitors.
Deregulated expression of HDAC9 in B cells promotes development of lymphoproliferative disease and lymphoma in mice.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Deregulated expression of HDAC9 in B cells promotes development of lymphoproliferative disease and lymphoma in mice.
Specimen part
View SamplesRecent studies of cortical pathology in secondary progressive multiple sclerosis have shown that a more severe clinical course and the presence of extended subpial grey matter lesions with significant neuronal/glial loss and microglial activation are associated with meningeal inflammation, including the presence of lymphoid-like structures in the subarachnoid space in a proportion of cases. To investigate the molecular consequences of pro-inflammatory and cytotoxic molecules diffusing from the meninges into the underlying grey matter, we carried out gene expression profiling analysis of the motor cortex from 20 post-mortem multiple sclerosis brains with and without substantial meningeal inflammation and 10 non-neurological controls. Gene expression profiling of grey matter lesions and normal appearing grey matter not only confirmed the substantial pathological cell changes, which were greatest in multiple sclerosis cases with increased meningeal inflammation, but also demonstrated the upregulation of multiple genes/pathways associated with the inflammatory response. In particular, genes involved in tumour necrosis factor (TNF) signalling were significantly deregulated in MS cases compared to controls.
Meningeal inflammation changes the balance of TNF signalling in cortical grey matter in multiple sclerosis.
Specimen part, Disease, Disease stage
View SamplesAnalysis of the transcriptome of zebrafish mononuclear myogenic cells (zMNCs) during myogenic differentiation. The main goal is to identify the similarities of zMNC myogenic differentiation with that of mammalian myoblast differentiation. Critical time points were used to identify a switch from the activity of cell proliferation genes to myogenic structural genes.
Isolation and transcriptome analysis of adult zebrafish cells enriched for skeletal muscle progenitors.
Specimen part, Time
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