Abstract
Long-standing UV exposure causes accumulation of degenerated elastic fibers in the dermis. This phenomenon is termed as solar elastosis and considered to be a histological marker of photoaging. The molecular mechanism by which the degenerated elastic fibers accumulate in the dermis by long-standing UV irradiation remains unknown, but three possible theories have been proposed; suppression of elastic fiber degradation (1)by leukocyte elastase inhibitor (elafin), (2)by advanced glycation end product (AGE) modification of elastin molecule, (3)by racemization of aspartic acid residue of elastin molecule. Leukocyte-derived elastase inhibitor (elafin) was found to (1)colocalize with elastic fiber accumulations in the dermis, (2)bind to elastin molecule via transglutaminase in vitro, (3)be induced by UVA irradiation, and (4)protect elastin molecule from elastolytic degradation. Abnormal accumulation of elastic fibers in solar elastosis therefore may be a secondary response preventing the elastic fibers from leukocyte elastase attack.
