|
KMID : 0984920090110010112
|
|
Journal of Skin Barrier Research
2009 Volume.11 No. 1 p.112 ~ p.122
|
|
|
Alteration in Aged Epidermal barrier
|
|
Lee Deborah
|
|
|
Abstract
|
|
|
Aged epidermis displays altered drug permeability, increased susceptibility to irritant contact dermatitis, and severe xerosis suggesting compromise of aged epidermal barrier. However, cutaneous barrier function is normal or even supernormal under basal conditions in aged skin. Functional pathology of the epidermis is revealed only after an active insult. The aged barrier is perturbed more readily and recovered more slowly in aged than in young skin. Global reduction of all key stratum corneum (SC) lipids, most profoundly cholesterol, with reduced activity of key enzymes and decreased extracellular lamellar bilayers could explain the impaired barrier recovery in aged epidermis. That is, main cause of impaired barrier function of advanced age(>75 years) is reduction of synthesis of key species of epidermal lipid. On the other hand, epidermal lipid synthesis is normal and the defective permeability barrier is associated with defective SC
acidity in moderately aged (50-80 years) skin. Decreased Na+/H+ antiporter (NHE1) accounts for the pH abnormality in moderately aged epidermis and lead to increased SC pH. The increased pH results in abnormal lipid-processing and delayed maturation of SC lamellar membrane. Moreover, increased pHdependent activation of serine protease accelerates corneodesmosome degradation leading to abnormal SC integrity. Delayed barrier recovery and abnormal lipid-processing in moderately aged mice were normalized by reacidification. Dry environment induces epidermal proliferation and scaling in both aged and young skin and no remarkable difference is found in skin barrier recovery of aged skin in a dry environment. Superimposition of photoaging on chronologically aged (CA) skin neither alter basal barrier function, nor
cause a further abnormality in barrier integrity but, cause a further abnormality in permeability barrier homeostasis in aged skin. Functional disturbance of SC in UV irradiated skin is not due to direct effect of UV radiation on SC, but just reflect secondary changes possibly caused by UV damage on underlying viable skin tissue that induce an epidermal proliferative response.
|
|
|
KEYWORD
|
|
|
Aged epidermis, Stratum corneum, Corneodesomosome, Photoaging
|
|
|
FullTexts / Linksout information
|
|
|
|
|
|
Listed journal information
|
|
|
|
|