Skin Barrier Formation And Caspase-14

The involvement of caspase-family members in programmed cell death and inflammation is well understood but, a function for caspase-14 had previously not been identified. Using caspase-14 knockout mice, Wim Declercq and colleagues show that caspase-14 is responsible for the correct degradation of profilaggrin and filaggrin. Filagrin is responsible for aggregating keratin and other proteins in the upper layers of the epidermis to form the stratum corneum -- a layer of flattened dead-cell remnants that creates a protective barrier for the skin. The controlled processing of profillagrin to produce filagrin ultimately maintains the integrity of the epidermis. In mice lacking caspase-14, their skin exhibits a defective stratum corneum and is more sensitive to water loss and UVB photodamage.

The identification of caspase-14 and its role in skin-barrier formation opens avenues for the pharmaceutical manipulation of this process to prevent the damage induced by UVB, the primary agent responsible for sunburn and skin ageing.

Author contact:

Wim Declercq (Ghent University, Belgium)
E-mail: wim.declercq@dmbr.ugent.be

Abstract available online.

(C) Nature Cell Biology press release.

Message posted by: Trevor M. D'Souza