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Expression data from post natal mouse aortic heart valves treated with all-trans retinoic acid or a retinoic acid receptor antagonist (LE540) relative to DMSO treated controls

ABSTRACT: Our lab has previously shown that treatment of murine heart valve explants with ATRA promotes calcification in vitro. In order to fully explore gene expression changes in the valve in response to ATRA or LE540, a high throughput microarray was performed. In this data set, we include expression data from dissected murine post natal aortic valve explants treated with ATRA or DMSO as a vehicle control. These data are used to obtain 432 probe sets that are differentially expressed in response to ATRA treatment, with 118 being downregulated and 314 increased.

ORGANISM(S): Mus musculus

PROVIDER: GSE40491 | GEO | 2012/08/31

SECONDARY ACCESSION(S): PRJNA174165

REPOSITORIES: GEO

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Project description:Targets of Retinoic Acid (RA) and 3,4-didehydroretinoic acid (ddRA) were identified in primary human epidermal keratinocytes grown in the presence of atRA or ddRA for 4 and 24 hours. Retinoids (natural forms and synthetic derivatives of vitamin A) are used as therapeutic agents for numerous skin diseases such as keratinization disorders (e.g. ichthyoses) and psoriasis. Two endogenous ligands for retinoic acid receptors exist, retinoic acid (atRA) and 3,4-didehydroretinoic acid (ddRA). In primary human epidermal keratinocytes many transcriptional targets for atRA are known, whereas the targets for ddRA are unknown. In an attempt to determine the targets, we compared the effect of atRA and ddRA on transcriptional profiles in undifferentiated and differentiating human primary keratinocytes. First, as expected, many genes were induced or suppressed in response to keratinocyte differentiation. Furthermore, the two retinoids affected substantially more genes in differentiated keratinocytes (more than 350) than in proliferating keratinocytes (20). In differentiating keratinocytes markers of cornification were suppressed suggesting a de-differentiating effect by the two retinoids. When comparing the expression profile of atRA to that of ddRA, no differently regulated genes were found. The array analysis also found that a minor number of miRNAs and a large number of non-coding transcripts were changed during differentiation and in response to the two retinoids. Furthermore, the expression of all, except one, genes known to cause autosomal recessive congenital ichthyosis (ARCI) were found to be induced by differentiation. These results comprehensively document that atRA and ddRA exert similar transcriptional changes in keratinocytes and also add new insights into the molecular mechanism influenced by retinoids in the epidermis. Furthermore, it suggests which ARCI patients could benefit from therapy with retinoids. Proliferating and differentiated keratinocytes were harvested after 4 and 24 hours after treatment with atRA, ddRA and vehicle for RNA extraction and hybridization on Affymetrix microarrays. Triplicate samples were generated for each time point and each treatment.

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Expression data from post natal mouse aortic heart valves treated with all-trans retinoic acid or a retinoic acid receptor antagonist (LE540) relative to DMSO treated controls

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