Defect of epidermal 12(S)-hydroxyeicosatetraenoic acid receptors in psoriasis

P. Arenberger, L. Kemény, T. Ruzicka

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

12-Hydroxyeicosatetraenoic acid (12-HETE) is assumed to play a central role in the pathophysiology of psoriasis. Since its effects in skin are mediated by specific high-affinity receptors, we studied the receptor characteristics in cultured epidermal cells from involved and apparently healthy skin of psoriasis patients by radioligand binding assay. Involved and uninvolved psoriatic epidermal cells showed a fourfold decrease in the number of 12-HETE binding sites as compared with normal healthy individuals and patients with atopic dermatitis, while receptor affinity remained unchanged. The decrease in receptor number was evident in psoriatic cells even in long-term culture and was not due to receptor down-regulation, defective response to interferon gamma or to protease degradation of receptor protein. The decrease in the number of 12-HETE receptors detectable even in clinically normal psoriatic skin functionally leads to diminished 12-HETE uptake and may thus represent a primary central molecular defect in the pathophysiology of the disease.

Original languageEnglish
Pages (from-to)235-243
Number of pages9
JournalEuropean Journal of Clinical Investigation
Volume22
Issue number4 I
Publication statusPublished - 1992

Fingerprint

Hydroxyeicosatetraenoic Acids
Psoriasis
Skin
Defects
Radioligand Assay
Atopic Dermatitis
Proteolysis
Interferon-gamma
Cultured Cells
Assays
Peptide Hydrolases
Down-Regulation
Binding Sites
Degradation
12-hydroxyeicosatetraenoic acid receptor
Proteins

Keywords

  • 12-HETE receptor defect
  • Keratinocytes
  • Psoriasis

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Defect of epidermal 12(S)-hydroxyeicosatetraenoic acid receptors in psoriasis. / Arenberger, P.; Kemény, L.; Ruzicka, T.

In: European Journal of Clinical Investigation, Vol. 22, No. 4 I, 1992, p. 235-243.

Research output: Contribution to journalArticle

@article{c0c985b11a114d859e23acaff5af0693,
title = "Defect of epidermal 12(S)-hydroxyeicosatetraenoic acid receptors in psoriasis",
abstract = "12-Hydroxyeicosatetraenoic acid (12-HETE) is assumed to play a central role in the pathophysiology of psoriasis. Since its effects in skin are mediated by specific high-affinity receptors, we studied the receptor characteristics in cultured epidermal cells from involved and apparently healthy skin of psoriasis patients by radioligand binding assay. Involved and uninvolved psoriatic epidermal cells showed a fourfold decrease in the number of 12-HETE binding sites as compared with normal healthy individuals and patients with atopic dermatitis, while receptor affinity remained unchanged. The decrease in receptor number was evident in psoriatic cells even in long-term culture and was not due to receptor down-regulation, defective response to interferon gamma or to protease degradation of receptor protein. The decrease in the number of 12-HETE receptors detectable even in clinically normal psoriatic skin functionally leads to diminished 12-HETE uptake and may thus represent a primary central molecular defect in the pathophysiology of the disease.",
keywords = "12-HETE receptor defect, Keratinocytes, Psoriasis",
author = "P. Arenberger and L. Kem{\'e}ny and T. Ruzicka",
year = "1992",
language = "English",
volume = "22",
pages = "235--243",
journal = "European Journal of Clinical Investigation",
issn = "0014-2972",
publisher = "Wiley-Blackwell",
number = "4 I",

}

TY - JOUR

T1 - Defect of epidermal 12(S)-hydroxyeicosatetraenoic acid receptors in psoriasis

AU - Arenberger, P.

AU - Kemény, L.

AU - Ruzicka, T.

PY - 1992

Y1 - 1992

N2 - 12-Hydroxyeicosatetraenoic acid (12-HETE) is assumed to play a central role in the pathophysiology of psoriasis. Since its effects in skin are mediated by specific high-affinity receptors, we studied the receptor characteristics in cultured epidermal cells from involved and apparently healthy skin of psoriasis patients by radioligand binding assay. Involved and uninvolved psoriatic epidermal cells showed a fourfold decrease in the number of 12-HETE binding sites as compared with normal healthy individuals and patients with atopic dermatitis, while receptor affinity remained unchanged. The decrease in receptor number was evident in psoriatic cells even in long-term culture and was not due to receptor down-regulation, defective response to interferon gamma or to protease degradation of receptor protein. The decrease in the number of 12-HETE receptors detectable even in clinically normal psoriatic skin functionally leads to diminished 12-HETE uptake and may thus represent a primary central molecular defect in the pathophysiology of the disease.

AB - 12-Hydroxyeicosatetraenoic acid (12-HETE) is assumed to play a central role in the pathophysiology of psoriasis. Since its effects in skin are mediated by specific high-affinity receptors, we studied the receptor characteristics in cultured epidermal cells from involved and apparently healthy skin of psoriasis patients by radioligand binding assay. Involved and uninvolved psoriatic epidermal cells showed a fourfold decrease in the number of 12-HETE binding sites as compared with normal healthy individuals and patients with atopic dermatitis, while receptor affinity remained unchanged. The decrease in receptor number was evident in psoriatic cells even in long-term culture and was not due to receptor down-regulation, defective response to interferon gamma or to protease degradation of receptor protein. The decrease in the number of 12-HETE receptors detectable even in clinically normal psoriatic skin functionally leads to diminished 12-HETE uptake and may thus represent a primary central molecular defect in the pathophysiology of the disease.

KW - 12-HETE receptor defect

KW - Keratinocytes

KW - Psoriasis

UR - http://www.scopus.com/inward/record.url?scp=0026509732&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026509732&partnerID=8YFLogxK

M3 - Article

C2 - 1323467

AN - SCOPUS:0026509732

VL - 22

SP - 235

EP - 243

JO - European Journal of Clinical Investigation

JF - European Journal of Clinical Investigation

SN - 0014-2972

IS - 4 I

ER -