Transcription profiling of human brain from X linked dystonia parkinsonism patients
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Gen Tamiya
PROVIDER: E-GEOD-3064 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:The temporal lobe is the cerebral cortex with critical function. The superior and middle gyrus of temporal lobe have been well studied, however, present perceptions on inferior temporal gyrus remains limited. The understanding of age-related protein profile change in human inferior temporal gyrus has not yet been well established. This 3-plex TMT labeled proteomic study is performed based on the human brain bank at the Chinese Academy of Medical Sciences & Peking Union Medical College. Age distribution of the donors ranges from 22 to 90 years old, and were assigned to three age groups: 20-50, 50-70, and 70-90 years of death age. In this ageing cohort, no neurodegenerative disorders or major stroke events were identified via standard neuropathological classification. Proteomics and bioinformatics strategies were applied to identify the perturbations of protein expression and associated pathways. Among all the ITG samples, 3113 proteins were isolated, with 37 proteins upregulated and 21 proteins downregulated.
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Project description:To identify molecular pathological alterations in AD brains, we performed interspecies comparative microarray analyses using RNAs prepared from postmortem human brain tissues donated for the Hisayama study and hippocampal RNAs from the triple-transgenic mouse model of AD (3xTg-AD) Three-way ANOVA of microarray data from frontal cortex, temporal cortex and hippocampus with presence/absence of AD and vascular dementia, and sex, as factors revealed that the gene expression profile is most significantly altered in the hippocampi of AD brains. Comparative analyses of the brains of AD patients and a mouse model of AD showed that genes involved in non-insulin dependent DM and obesity were significantly altered in both, as were genes related to psychiatric disorders and Alzheimer’s disease. We prepared RNA samples from the gray matter of frontal and temporal cortices and hippocampi derived from 88 postmortem brains, among which 26 cases were pathologically diagnosed as having AD or an AD-like disorder. High-quality RNA (RIN≧6.9) samples were subjected to microarray analysis using the Affymetrix Human Gene 1.0 ST platform, and only those results that passed examinations for quality assurance and quality control of the Human Gene 1.0 ST arrays were retrieved. In total, we obtained gene expression profiles from the following samples: 33 frontal cortex samples, among which 15 were from AD patients; 29 temporal cortex samples, among which 10 were from AD patients; 17 hippocampus samples, among which seven were from AD patients
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Project description:Gonadotrope or null cell pituitary tumors present clinically with signs of hypogonadism and hypopituitarism, together with visual disturbances due to mass effects. Since there are no medical therapies, surgery and/or radiation are the only therapeutic options. To identify dysregulated genes and/or pathways that may play a role in tumorigenesis and/ or progression, molecular profiling was performed on 14 gonadotrope tumors and 9 normal human pituitaries from autopsy samples. Principle component analysis (PCA) revealed clear discrimination between tumor and normal pituitary gene expression profiles. Bioinformatic analysis identified specific genes and pathways that were highly differentially regulated, including a cohort of putative downstream effectors of p53 were repressed in gonadotrope pituitary tumors, including GADD45β, GADD45γ and Reprimo with concomitant downregulation of the upstream regulator, PLAGL1. PLAGL1 reexpression in gonadotrope cells did not directly modulate the downstream targets. Further functional analysis of GADD45β was performed. Overexpression of GADD45β in mouse gonadotrope cells blocked proliferation, increased rates of apoptosis in response to growth factor withdrawal and increased colony formation in soft agar. In contrast to prior studies with GADD45γ, methylation interference assays showed no evidence of epigenetic modification of the GADD45β promoter in pituitary tumors. Thus, our data suggest that many components downstream of p53 are suppressed in gonadotrope pituitary tumors. A novel candidate, GADD45β is low in tumors and reexpression blocks proliferation, survival and tumorigenesis in gonadotrope cells. Unlike GADD45γ, GADD45β is not methylated to block its expression. Together these studies identify new targets and mechanisms to explore concerning pituitary tumor initiation and progression. To elucidate mechanisms involved in pituitary tumorigenesis and progression, we performed individual gene expression microarray analysis using Affy U133 Plus 2.0 GeneChips comparing 14 gonadotrope tumors with 9 normal pituitary samples obtained at autopsy.
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Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
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