Epp, Nikolas and Fuerstenberger, Gerhard and Mueller, Karsten and de Juanes, Silvia and Leitges, Michael and Hausser, Ingrid and Thieme, Florian and Liebisch, Gerhard and Schmitz, Gerd and Krieg, Peter (2007) 12R-lipoxygenase deficiency disrupts epidermal barrier function. JOURNAL OF CELL BIOLOGY, 177 (1). pp. 173-182. ISSN 0021-9525, 1540-8140
Full text not available from this repository. (Request a copy)Abstract
12R-lipoxygenase (12R-LOX) and the epidermal LOX-3 (eLOX-3) constitute a novel LOX pathway involved in terminal differentiation in skin. This view is supported by recent studies showing that inactivating mutations in 12R-LOX and eLOX-3 are linked to the development of autosomal recessive congenital ichthyosis. We show that 12R-LOX deficiency in mice results in a severe impairment of skin barrier function. Loss of barrier function occurs without alterations in proliferation and stratified organization of the keratinocytes, but is associated with ultrastructural anomalies in the upper granular layer, suggesting perturbance of the assembly/extrusion of lamellar bodies. Cornified envelopes from skin of 12R-LOX-deficient mice show increased fragility. Lipid analysis demonstrates a disordered composition of ceramides, in particular a decrease of ester-bound ceramide species. Moreover, processing of profilaggrin to monomeric filaggrin is impaired. This study indicates that the 12R-LOX-eLOX-3 pathway plays a key role in the process of epidermal barrier acquisition by affecting lipid metabolism, as well as protein processing.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | CAUSE ICHTHYOSIS VULGARIS; CHROMOSOMAL LOCALIZATION; MOLECULAR-CLONING; ATOPIC-DERMATITIS; GENOMIC STRUCTURE; TIGHT JUNCTIONS; WATER-LOSS; SKIN; GENE; LIPOXYGENASES; - |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Klinische Chemie und Laboratoriumsmedizin |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 15 Dec 2020 16:08 |
| Last Modified: | 15 Dec 2020 16:08 |
| URI: | https://pred.uni-regensburg.de/id/eprint/32896 |
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