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Involvement of the ABC-transporter ABCC1 and the sphingosine 1-phosphate receptor subtype S1P(3) in the cytoprotection of human fibroblasts by the glucocorticoid dexamethasone

Academic Article
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Overview

authors

  • Nieuwenhuis, B.
  • Luth, A.
  • Chun, Jerold
  • Huwiler, A.
  • Pfeilschifter, J.
  • Schafer-Korting, M.
  • Kleuser, B.

publication date

  • June 2009

journal

  • Journal of Molecular Medicine-JMM  Journal

abstract

  • Glucocorticoids (GC) represent the most commonly used drugs for the treatment of acute and chronic inflammatory skin diseases. However, the topical long-term therapy of GC is limited by the occurrence of skin atrophy. Most interestingly, although GC inhibit proliferation of human fibroblasts, they exert a pronounced anti-apoptopic action. In the present study, we further elucidated the molecular mechanism of the GC dexamethasone (Dex) to protect human fibroblasts from programmed cell death. Dex not only significantly alters the expression of the cytosolic isoenzyme sphingosine kinase 1 but also initiated an enhanced intracellular formation of the sphingolipid sphingosine 1-phosphate (S1P). Investigations using S1P (3) ((-/-)) -fibroblasts revealed that this S1P-receptor subtype is essential for the Dex-induced cytoprotection. Moreover, we demonstrate that the ATP-binding cassette (ABC)-transporter ABCC1 is upregulated by Dex and may represent a crucial carrier to transport S1P from the cytosol to the S1P(3)-receptor subtype.

subject areas

  • Apoptosis
  • Cells, Cultured
  • Cytoprotection
  • Dexamethasone
  • Fibroblasts
  • Glucocorticoids
  • Humans
  • Multidrug Resistance-Associated Proteins
  • Receptors, Lysosphingolipid
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Research

keywords

  • ABC-transporter
  • Dexamethasone
  • Glucocorticoids
  • S1P-receptor subtypes
  • Sphingosine 1-phosphate
  • Sphingosine kinase
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Identity

International Standard Serial Number (ISSN)

  • 0946-2716

Digital Object Identifier (DOI)

  • 10.1007/s00109-009-0468-x

PubMed ID

  • 19370318
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Additional Document Info

start page

  • 645

end page

  • 657

volume

  • 87

issue

  • 6

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