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Circadian gene expression in the primate adrenal gland

ABSTRACT: Circadian regulation of gene expression in central and peripheral tissue has been studied in mice. The biomedical implications of this findings led us to the development of a model in which to study the circadian mechanisms underlying primate physiology. The objective of this experiment has been to identify genes that are circadianly regulated in the monkey (macaca mulatta) adrenal gland. We analyzed the data using three filters: the first one for presence in at least three out of six time points (presence call=P, P value<0.05). The second one for high amplitude oscillations, using the coefficient of variation with a cutt of value of 0.2 (selecting probesets above that value). The last one for circadian expression, calculating the correlation of each curve to cosine curves of 24h periodicity and defined phases with increments of 10 minutes from 0 to 24h. After two filtrations, the probesets obtained were identified using gene ID, PubMed accession number, and description, and clustered into well-known pathways. Identification of clock genes was used as an internal control for the determination of phase distribution of the transcripts across the day. Part of the array data has been validated by sq PCR, real time-PCR and immunohistochemistry, with succesful results. This study provides evidences for circadian mechanisms of gene expression in primate tissue, in vivo. Keywords = primate Keywords = circadian rhythm Keywords = adrenal gland Keywords: time-course

ORGANISM(S): Homo sapiens Macaca mulatta

PROVIDER: GSE2703 | GEO | 2005/11/02

SECONDARY ACCESSION(S): PRJNA92349

REPOSITORIES: GEO

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Project description:Abstract submitted to the Journal of clinical encodcrinology and metabolism: The molecular mechanisms responsible for the ectopic expression of the GIP receptor in the adrenal cortex of patients with GIP-dependent Cushing’s syndrome (CS) are unknown. Chronic adrenal stimulation by ACTH in Cushing’s disease (CD) or by GIP in GIP-dependent AIMAH both lead to induction of a set of genes which stimulate adrenal proliferation and steroidogenesis. The objective of this study was to compare the whole genome expression profile of adrenal glands of five cases of GIP-dependent bilateral macronodular adrenal hyperplasia with CS, one case of GIP-dependent adenoma, compared to five cases of ACTH-dependant hyperplasias (CD) and a pool of adrenals from 62 normal individuals. We used the genome-spanning Affymetrix U133 plus 2.0 microarray oligochips to identify genes differentially expressed specifically in GIP-dependent CS and which would be candidate genes implicated in the ectopic expression of the GIP receptor in the adrenal cortex. After data normalization and filtering, genes with differential expression were identified with a multi-step statistical analysis involving a student’s t-test, a filter on flags and a SAM analysis. A total of 721 probesets were thus isolated with intensity levels robustly related to the presence of a GIP-dependent hyperplasia. We performed a functional classification to further define potentially important biological processes and signaling mechanism for the formation of GIP-dependent AIMAH. Various probesets were related to metabolic processes, cell-surface and intracellular signaling, tumorigenesis, transport and transcription factors. The most relevant genes had their expression profile confirmed by real-time RT-PCR. This study reports an extensive series of potentially novel targets in the identification of the molecular mechanisms of ectopic expression of the GIP-receptor in this pathology. Keywords: Comparative genomic analysis

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Circadian gene expression in the primate adrenal gland

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