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The "Caveolae Brake Hypothesis" and the Epidermal Barrier

Truus Roelandt, Christina Giddelo, Carol Heughebaert, Geertrui Denecker UGent, Melanie Hupe, Debra Crumrine, Andy Kusuma, Marek Haftek, Diane Rosseeuw and Wim Declercq UGent, et al. (2009) JOURNAL OF INVESTIGATIVE DERMATOLOGY. 129(4). p.927-936
abstract
Epidermal permeability barrier formation depends upon lamellar body (LB) secretion/fusion with the apical plasma membrane (APM) of outermost stratum granulosum (SG) cell, creating cholesterol/glycosphingolipid-enriched lipid rafts-like domains. We found that the dimensions of these domains are comparable to lipid raft in other cell types; and that acute barrier disruption regulates their size and dynamics. To assess the function of these LB-derived raft-like domains, we assessed APM dynamics and barrier recovery in methyl-beta-cyclodextrin (M beta CD)-treated hairless mice and caveolin-1 knockouts (cav-1(-/-)). MbCD treatment impaired APM raft-like domain formation and barrier recovery. Accelerated barrier recovery is observed in cav-1(-/-) in parallel with expansion of raft-like domains. Barrier abrogation of normal epidermis resulted in translocation of cav-1 from the cytoplasm to raft-like membrane domains, restricting further raft-like domain formation and initiating terminal differentiation. Inhibition of LB secretion by monensin and absence of cav-1 delayed terminal differentiation. Furthermore, cav-1(-/-) mice exhibited an increased propensity to develop experimentally induced epidermal hyperplasia correlating with lipid raft persistence. Finally, the epidermal hyperplasia in psoriasis and Netherton syndrome is paralleled by increased lipid raft formation. These studies demonstrate that cav-1 delivery to the APM by LB trafficking to APM "brakes'' further LB secretion, signals terminal differentiation, and regulates epidermal hyperproliferation.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
journal title
JOURNAL OF INVESTIGATIVE DERMATOLOGY
J. Invest. Dermatol.
volume
129
issue
4
pages
927 - 936
Web of Science type
Article
Web of Science id
000264994200017
JCR category
DERMATOLOGY
JCR impact factor
5.543 (2009)
JCR rank
1/48 (2009)
JCR quartile
1 (2009)
ISSN
0022-202X
DOI
10.1038/jid.2008.328
language
English
UGent publication?
yes
classification
A1
id
632525
handle
http://hdl.handle.net/1854/LU-632525
date created
2009-05-19 12:01:42
date last changed
2012-06-26 14:31:43
@article{632525,
  abstract     = {Epidermal permeability barrier formation depends upon lamellar body (LB) secretion/fusion with the apical plasma membrane (APM) of outermost stratum granulosum (SG) cell, creating cholesterol/glycosphingolipid-enriched lipid rafts-like domains. We found that the dimensions of these domains are comparable to lipid raft in other cell types; and that acute barrier disruption regulates their size and dynamics. To assess the function of these LB-derived raft-like domains, we assessed APM dynamics and barrier recovery in methyl-beta-cyclodextrin (M beta CD)-treated hairless mice and caveolin-1 knockouts (cav-1(-/-)). MbCD treatment impaired APM raft-like domain formation and barrier recovery. Accelerated barrier recovery is observed in cav-1(-/-) in parallel with expansion of raft-like domains. Barrier abrogation of normal epidermis resulted in translocation of cav-1 from the cytoplasm to raft-like membrane domains, restricting further raft-like domain formation and initiating terminal differentiation. Inhibition of LB secretion by monensin and absence of cav-1 delayed terminal differentiation. Furthermore, cav-1(-/-) mice exhibited an increased propensity to develop experimentally induced epidermal hyperplasia correlating with lipid raft persistence. Finally, the epidermal hyperplasia in psoriasis and Netherton syndrome is paralleled by increased lipid raft formation. These studies demonstrate that cav-1 delivery to the APM by LB trafficking to APM {\textacutedbl}brakes'' further LB secretion, signals terminal differentiation, and regulates epidermal hyperproliferation.},
  author       = {Roelandt, Truus and Giddelo, Christina and Heughebaert, Carol and Denecker, Geertrui and Hupe, Melanie and Crumrine, Debra and Kusuma, Andy and Haftek, Marek and Rosseeuw, Diane and Declercq, Wim and Feingold, Kenneth R. and Elias, Peter M. and Hachem, Jean-Pierre},
  issn         = {0022-202X},
  journal      = {JOURNAL OF INVESTIGATIVE DERMATOLOGY},
  language     = {eng},
  number       = {4},
  pages        = {927--936},
  title        = {The {\textacutedbl}Caveolae Brake Hypothesis{\textacutedbl} and the Epidermal Barrier},
  url          = {http://dx.doi.org/10.1038/jid.2008.328},
  volume       = {129},
  year         = {2009},
}

Chicago
Roelandt, Truus, Christina Giddelo, Carol Heughebaert, Geertrui Denecker, Melanie Hupe, Debra Crumrine, Andy Kusuma, et al. 2009. “The ‘Caveolae Brake Hypothesis’ and the Epidermal Barrier.” Journal of Investigative Dermatology 129 (4): 927–936.
APA
Roelandt, T., Giddelo, C., Heughebaert, C., Denecker, G., Hupe, M., Crumrine, D., Kusuma, A., et al. (2009). The “Caveolae Brake Hypothesis” and the Epidermal Barrier. JOURNAL OF INVESTIGATIVE DERMATOLOGY, 129(4), 927–936.
Vancouver
1.
Roelandt T, Giddelo C, Heughebaert C, Denecker G, Hupe M, Crumrine D, et al. The “Caveolae Brake Hypothesis” and the Epidermal Barrier. JOURNAL OF INVESTIGATIVE DERMATOLOGY. 2009;129(4):927–36.
MLA
Roelandt, Truus, Christina Giddelo, Carol Heughebaert, et al. “The ‘Caveolae Brake Hypothesis’ and the Epidermal Barrier.” JOURNAL OF INVESTIGATIVE DERMATOLOGY 129.4 (2009): 927–936. Print.