Document Detail


Localization of epidermal sphingolipid synthesis and serine palmitoyl transferase activity: alterations imposed by permeability barrier requirements.
MedLine Citation:
PMID:  7598529     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Sphingolipids, the predominant lipid species in mammalian stratum corneum play, a central role in permeability barrier homeostatis. Prior studies have shown that the epidermis synthesizes abundant sphingolipids, a process regulated by barrier requirements, and that inhibition of sphingolipid synthesis interferes with barrier homeostasis. To investigate further the relationship between epidermal sphingolipid metabolism and barrier function, we localized sphingolipid synthetic activity in murine epidermis under basal conditions, and following acute (acetone treatment) or chronic (essential fatty acid deficiency, EFAD) barrier perturbation, using dithiothreitol and/or the staphylococcal epidermolytic toxin to isolate the lower from the outer epidermis. Under basal conditions, both the activity of serine palmitoyl transferase (SPT), the rate-limiting enzyme of sphingolipid synthesis, and the rates of 3H-H2O incorporation into sphingolipids were nearly equivalent in the lower and the outer epidermis. Following acute barrier perturbation, SPT activity increased significantly in both the lower (35%; P < 0.05) and the outer epidermal layers (60%; P < 0.01). The rates of 3H-H2O incorporation into each major sphingolipid family, including ceramides, glucosylceramides and sphingomyelin, increased significantly in both the lower and the outer epidermis of treated flanks after acute barrier disruption. Finally, SPT activity was modestly elevated (20%; P < 0.01) in the lower but not in the outer epidermis of EFAD animals. These studies demonstrate the ability of both lower and outer epidermal cells to generate sphingolipids, and that permeability barrier homeostatic mechanisms appear to differentially regulate SPT activity and sphingolipid synthesis in the lower and the outer epidermis in response to acute and chronic barrier perturbation.(ABSTRACT TRUNCATED AT 250 WORDS)
Authors:
W M Holleran; W N Gao; K R Feingold; P M Elias
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Archives of dermatological research     Volume:  287     ISSN:  0340-3696     ISO Abbreviation:  Arch. Dermatol. Res.     Publication Date:  1995  
Date Detail:
Created Date:  1995-08-03     Completed Date:  1995-08-03     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  8000462     Medline TA:  Arch Dermatol Res     Country:  GERMANY    
Other Details:
Languages:  eng     Pagination:  254-8     Citation Subset:  IM    
Affiliation:
Dermatology Service, Veterans Administration Medical Center, San Francisco, CA 94121, USA.
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MeSH Terms
Descriptor/Qualifier:
Acetone / toxicity
Acyltransferases / metabolism*
Animals
Cholesterol / biosynthesis
Epidermis / drug effects,  metabolism*
Fatty Acids, Essential / deficiency
Homeostasis
Male
Mice
Mice, Hairless
Permeability / drug effects
Serine C-Palmitoyltransferase
Sphingolipids / biosynthesis*
Grant Support
ID/Acronym/Agency:
AR 19098/AR/NIAMS NIH HHS; AR 39448/AR/NIAMS NIH HHS; AR 39639/AR/NIAMS NIH HHS
Chemical
Reg. No./Substance:
0/Fatty Acids, Essential; 0/Sphingolipids; 57-88-5/Cholesterol; 67-64-1/Acetone; EC 2.3.-/Acyltransferases; EC 2.3.1.50/Serine C-Palmitoyltransferase; EC 2.3.1.50/Sptlc1 protein, mouse

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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