Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Early life growth and gene profile changes during childhood

ABSTRACT: To compare early life exposures to see if they are associated with persistent molecular changes at the transcriptional level. Subjects were drawn from the Newcastle Pre-Term Birth Growth Study. A randomised, controlled trial to look at the effect on growth of dietary manipulation after hospital discharge. 23 chips with 4 conditions with factors sex and growth status (slow/rapid). Each condition has 6 replicates except for {male, rapid growth} which has 5 replicates.

ORGANISM(S): Homo sapiens

SUBMITTER: Simon Cockell

PROVIDER: E-GEOD-22013 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Publications

Postnatal growth and DNA methylation are associated with differential gene expression of the TACSTD2 gene and childhood fat mass.

Groom Alexandra A Potter Catherine C Swan Daniel C DC Fatemifar Ghazaleh G Evans David M DM Ring Susan M SM Turcot Valerie V Pearce Mark S MS Embleton Nicholas D ND Smith George Davey GD Mathers John C JC Relton Caroline L CL

Diabetes 20111221 2

Rapid postnatal growth is associated with increased risk of childhood adiposity. The aim of this study was to establish whether this pathway is mediated by altered DNA methylation and gene expression. Two distinct cohorts, one preterm (n=121) and one term born (n=6,990), were studied. Exploratory analyses were performed using microarrays to identify differentially expressed genes in whole blood from children defined as "slow" (n=10) compared with "rapid" (n=10) postnatal (term to 12 weeks correc ...[more]

PMID: 22190649

Similar Datasets

Project description:Background: The heteroplasmic mitochondrial DNA (mtDNA) mutation A3243G causes the MELAS syndrome as one of the most frequent mitochondrial diseases. The process of reconfiguration of nuclear gene expression profile to accommodate cellular processes to the functional status of mitochondria might be a key to MELAS disease manifestation and could contribute to its diverse phenotypic presentation. Objective: To determine master regulatory protein networks and disease-modifying genes in MELAS syndrome. Methods: Analyses of whole blood transcriptomes from 10 MELAS patients using a novel strategy by combining classic Affymetrix oligonucleotide microarray profiling with regulatory and protein interaction network analyses. Results and Interpretation: Hierarchical cluster analysis elucidated that the relative abundance of mutant mtDNA molecules is decisive for the nuclear gene expression response. Further analyses confirmed not only transcription factors already known to be involved in mitochondrial diseases (such as TFAM), but also detected the hypoxia-inducible factor 1α (HIF-1α)/HIF-1β complex, nuclear factor Y (NF-Y) and CREB-related transcription factors as novel master regulators for reconfiguration of nuclear gene expression in response to the MELAS mutation. Correlation analyses of gene alterations and clinico-genetic data detected significant correlations between A3243G-induced nuclear gene expression changes and mutant mtDNA load as well as disease characteristics. These potential disease-modifying genes influencing the expression of the MELAS phenotype are mainly related to clusters primarily unrelated to cellular energy metabolism, but important for nucleic acid and protein metabolism, and signal transduction. Our data thus provide a framework to search for new pathogenetic concepts and potential therapeutic approaches to treat the MELAS syndrome. Peripheral blood samples were collected from ten A3243G MELAS patients and twenty age- and sex-matched healthy controls (2 controls for each patient). The patient cohort consisted of 4 females and 6 males, mean±s.e.m. age was 44.1±11.9 years (range: 22–63 years), mean±s.e.m. age at disease onset was 27.1±4.9 years (range: 13–55 years), mean±s.e.m. disease duration was 19.0±4.7 years (range: 4–43 years), and disease severity measured by the ‘Newcastle Mitochondrial Disease Adult Scale’ (NMDAS) 8 ranging from 0.0 (no symptoms) to 1.0 (maximum score) was 0.26±0.05 (range: 0.02–0.54).

Dataset Information

Early life growth and gene profile changes during childhood

Publications

Postnatal growth and DNA methylation are associated with differential gene expression of the TACSTD2 gene and childhood fat mass.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets