Please note that we have stopped the regular imports of Gene Expression Omnibus (GEO) data into ArrayExpress. This may not be the latest version of this experiment.
E-GEOD-41742 - Expression changes between loricrin knockout and wildtype P0
Released on 28 June 2013, last updated on 2 June 2014
The loss of loricrin, a major component of the cornified envelope, results in a delay of epidermal barrier formation. Therefore, the living layers of the epidermis are aberrantly exposed to late-stage amniotic fluid, which may serve as the signal to upregulate genes that functionally compensate for the loss of loricrin. Consistent with this hypothesis, metabolomic studies revealed marked changes in amniotic fluid between E14.5 and E16.5 dpc. In addition, we discovered that the Nrf2/Keap1 pathway detects these compositional changes and directly upregulates the expression of genes involved in the compensatory response, thus ensuring postnatal survival. In support of this finding, we demonstrate that genetically blocking the Nrf2 pathway abolishes the compensatory response, and preemptively activating Nrf2 pharmacologically rescues the delay in barrier formation in utero. Our findings reveal that the functions of Nrf2 and the composition of amniotic fluid have co-evolved to ensure the formation of a functional barrier. 1 sample with one replicate for each genotype was performed for both loricrin knockout and wildtype
transcription profiling by array
Dennis R. Roop <email@example.com>, Dennis Roop
Amniotic fluid activates the nrf2/keap1 pathway to repair an epidermal barrier defect in utero. Huebner AJ, Dai D, Morasso M, Schmidt EE, Schï¿½fer M, Werner S, Roop DR. , PMID:23237955