Expression data from adult mouse epidermis upon tamoxifen induced inactivation of Alox12b

Autosomal recessive congenital ichthyoses (ARCI) are a group of non-syndromic congenital keratinization disorders including harlequin ichthyosis, lamellar ichthyosis, and congenital ichthyosiform erythroderma with a total prevalence of 1:200,000. Affected individuals who are often born as collodion babies present with generalized scaling of the skin. This reflects a physical compensation for the defective cutaneous permeability barrier underlying all ichthyoses. Inactivity of 12R-lipoxygenase (12R-LOX) is a frequent cause of ARCI. Epidermis-specific conditional knockout of Alox12b encoding 12R-LOX was established in mice using the Cre-Lox system. Tamoxifen-induced Alox12b inactivation in mouse skin caused an ichthyosis-like phenotype. We used microarray to compare the gene expression profile in the epidermis of mice after tamoxifen induced Alox12b inactivation with that of control animals. Inactivation of Alox12b was associated with the upregulation of genes involved in keratinization, cholesterol biosynthesis, and Fc-epsilon receptor signaling. Alox12b inactivation in keratinocytes of 8-week old Alox12bfl/fl/K14-Cre mice was induced by repeated intraperitoneal injection of tamoxifen. Homozygous floxed littermates (Alox12bfl/fl) treated in parallel served as controls. 6 days after tamoxifen treatment the mice were sacrified and epidermis was harvested for RNA extraction and hybridization on Affymetrix microarrays.