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J. Biol. Chem., Vol. 277, Issue 4, 2916-2922, January 25, 2002
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From the Cholesterol is a key lipid in the
stratum corneum, where it is critical for permeability barrier
homeostasis. The epidermis is an active site of cholesterol synthesis,
but inhibition of epidermal cholesterol synthesis with topically
applied statins only modestly affects epidermal permeability barrier
function, suggesting a possible compensatory role for extraepidermal
cholesterol. Scavenger receptor class B type I (SR-BI) is a recently
described cell surface receptor for high density lipoproteins (HDL)
that mediates the selective uptake of cholesterol esters from
circulating HDL. In the present study, we demonstrate that SR-BI is
present in cultured human keratinocytes and that calcium-induced
differentiation markedly decreases SR-BI levels. Additionally, the cell
association of [3H]cholesterol-labeled HDL
decreased in differentiated versus undifferentiated keratinocytes. Furthermore, the inhibition of cholesterol synthesis with simvastatin resulted in a 3-4-fold increase in both SR-BI mRNA and protein levels, whereas conversely, addition of
25-hydroxycholesterol suppressed SR-BI levels by approximately 50%.
SR-BI mRNA is also expressed in murine epidermis, increasing by
50% in parallel with cholesterol requirements following acute barrier
disruption. Because the increase is completely blocked by occlusion
with a vapor-impermeable membrane, changes in epidermal SR-BI
expression are regulated specifically by barrier requirements. Lastly,
using immunofluorescence we demonstrated that SR-BI is present in human
epidermis predominantly in the basal layer and increases following
barrier disruption. In summary, the present study demonstrates first
that SR-BI is expressed in keratinocytes and regulated by cellular
cholesterol requirements, suggesting that it plays a role in
keratinocyte cholesterol homeostasis. Second, the increase in SR-BI
following barrier disruption suggests that SR-BI expression increases
to facilitate cholesterol uptake leading to barrier restoration.
Scavenger Receptor Class B Type I Is Expressed in Cultured
Keratinocytes and Epidermis
REGULATION IN RESPONSE TO CHANGES IN CHOLESTEROL HOMEOSTASIS AND
BARRIER REQUIREMENTS*
§¶,
**,§,§,§, and**
Dermatology and Medical (Metabolism)
Services, Department of Veterans Affairs Medical Center, San Francisco,
California 94121, the Departments of § Dermatology and
** Medicine, University of California, San Francisco School
of Medicine, San Francisco, California 94143, and ¶ R & D
Department of Dermatological Science, POLA Laboratories, POLA
Chemical Industries Inc., 560 Kashio-cho, Totsuka-ku,
Yokohama 244-0812 Japan
*
This work was supported by National Institutes of Health
Grants HD 29706, AR 39639, AR 29706, and PO039448 and by Veterans Affairs Research Funding.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Metabolism Section,
Dept. of Veterans Affairs Medical Center, 4150 Clement St., Box 111F,
San Francisco, CA 94121. Tel.: 415-750-2005; Fax: 415-750-6927; E-mail: kfngld@itsa.ucsf.edu.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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