Unknown,Transcriptomics,Genomics,Proteomics

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Genome-wide gene expression in Dupuytrenâs disease

ABSTRACT: We compared the whole-genome expression profiles of primary tissue samples from Dupuytren patients and controls. The aim was to identify differential expressed genes in the disease tissue and to identify pathways and networks altered in DupuytrenÂ´s disease. Total RNA was obtained from disease and control primary tissue samples. Twelve Dupuytren Samples were compared with 12 samples from age and gender matched controls for genome-wide differential expression.

ORGANISM(S): Homo sapiens

SUBMITTER: Kerstin Becker

PROVIDER: E-GEOD-75152 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Peripheral blood samples of patients with acute myocardial infarction were matched with those of control patients to identify possible differences in corresponding gene expression profiles. The controls were matched to cases based on gender, age, status of diabetes mellitus and smoking status. Six months cardiovascular survival status of the cases was used to identify two distinct subgroups among the cases. Linear models for microarray data (M-bM-^@M-^XlimmaM-bM-^@M-^Y) were employed to identify differential gene expression. Shrunken centroids technique helped in identifying the subsets of differentially expressed genes with predictive properties in independent samples. Predictive properties were evaluated using bootstrap sampling. Using the limma modeling with the log-fold change threshold of one (clinical significance) and StoreyM-bM-^@M-^Ys q-value approach (statistical significance), sixty transcripts were found to be both clinically and statistically differentially expressed among the cases not surviving the follow-up period relative to controls, while no such transcripts were observed among other surviving cases. The two subgroups of cases exhibited fourteen differentially expressed transcripts. Predictive modeling indicated sixteen out of sixty transcripts to best discriminate between the controls and cases who died during the follow-up period from cardiovascular causes, while for the surviving cases the already non-significant set of transcripts could not be further reduced. Eleven out of fourteen transcripts were found to best discriminate between the two groups of cases using shrunken centroids. The study identified genes, which were differentially expressed during the acute myocardial infarction, including those associated with short-term fatality of the cases. The genome-wide study used matched case-control design, with 97 samples of 90 patients in three disease groups. Matched control samples were used and several (7) technical replicates were performed.

Project description:Primary mitochondrial respiratory chain (RC) diseases are heterogeneous in etiology and manifestations but collectively impair cellular energy metabolism. To identify a common cellular response to RC disease, systems biology level transcriptome investigations were performed in human RC disease skeletal muscle and fibroblasts. Global transcriptional and post-transcriptional dysregulation in a tissue-specific fashion was identified across diverse RC complex and genetic etiologies. RC disease muscle was characterized by decreased transcription of cytosolic ribosomal proteins to reduce energy-intensive anabolic processes, increased transcription of mitochondrial ribosomal proteins, shortened 5'-UTRs to improve translational efficiency, and stabilization of 3'-UTRs containing AU-rich elements. These same modifications in a reversed direction typified RC disease fibroblasts. RC disease also dysregulated transcriptional networks related to basic nutrient-sensing signaling pathways, which collectively mediate many aspects of tissue-specific cellular responses to primary RC disease. These findings support the utility of a systems biology approach to improve mechanistic understanding of mitochondrial RC disease. To identify a common cellular response to primary RC that might improve mechanistic understanding and lead to targeted therapies for human RC disease, we performed collective transcriptome profiling in skeletal muscle biopsy specimens and fibroblast cell lines (FCLs) of a diverse cohort of human mitochondrial disease subjects relative to controls. Systems biology investigations of common cellular responses to primary RC disease revealed a collective pattern of transcriptional, post-transcriptional and translational dysregulation occurring in a highly tissue-specific fashion. Affymetrix Human Exon 1.0ST microarray analysis was performed on 29 skeletal muscle samples and Fibroblast cell lines from mitochondrial disease patients and age- and gender-matched controls.

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Genome-wide gene expression in Dupuytrenâs disease

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Genome-wide gene expression in Dupuytrenâs disease

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OmicsDI is part of the ELIXIR infrastructure

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Genome-wide gene expression in Dupuytrenâs disease