23 February 2006 Using FLIM in the study of permeability barrier function of aged and young skin
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Abstract
Aged skin commonly is afflicted by inflammatory skin diseases or xerosis/eczema that can be triggered or exacerbated by impaired epidermal permeability barrier homeostasis. It has been previously described a permeability barrier defect in humans of advanced age (> 75 years), which in a murine analog >18 mos, could be attributed to reduced lipid synthesis synthesis. However, the functional abnormality in moderately aged mice is due not to decreased lipid synthesis, but rather to a specific defect in stratum corneum (SC) acidification causing impaired lipid processing processing. Endogenous Na+/H+ antiporter (NHE1) level was found declined in moderately aged mouse epidermis. This acidification defect leads to perturbed permeability barrier homeostasis through more than one pathways, we addressed suboptimal activation of the essential, lipid-processing enzyme, β-glucocerebrosidase (BGC) is linked to elevated SC pH. Finally, the importance of the epidermis acidity is shown by the normalization of barrier function after exogenous acidification of moderately aged skin.
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P. Xu, P. Xu, E. H. Choi, E. H. Choi, M. Q. Man, M. Q. Man, D. Crumrine, D. Crumrine, T. Mauro, T. Mauro, P. Elias, P. Elias, } "Using FLIM in the study of permeability barrier function of aged and young skin", Proc. SPIE 6089, Multiphoton Microscopy in the Biomedical Sciences VI, 60890Q (23 February 2006); doi: 10.1117/12.660985; https://doi.org/10.1117/12.660985
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