Crosstalk of sterol-dependent and non-sterol-dependent signaling in human monocytes after in vitro addition of LDL

Ildikó Seres, Gabriella Fóris, Éva Kovács, Dénes Páll, Zsuzsa Varga, Zoltán Balogh, György Paragh

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

The aim of the present study was to investigate low density lipoprotein (LDL)-induced, non-sterol-dependent signaling and its possible role in cholesterol balance. LDL in 10 μg ml-1 concentration could induce inositol trisphosphate (IP3) and Ca2+ signal generation through a pertussis toxin (PT) sensitive G protein in human monocytes. The increase in [Ca2+]i was derived from the intracellular pools. LDL also induced activation and translocation of protein kinase C (PKC) into the cell membrane, by processes, which were significantly inhibited in the first 20 min by preincubation with PT and PKC-inhibitor H-7. The PKC-activating phorbol-12-myristate-13-acetate (PMA), differently from LDL, enhanced the LDL-receptor (LDL-R)-mediated binding and degradation of [125I]LDL, but inhibited endogenous cholesterol synthesis, and both effects were inhibited by H-7. The LDL-induced inhibition of binding and degradation of [ 125I]LDL was not affected by H-7, whereas decreased cholesterol synthesis was counteracted by H-7. These results suggest the existence of a non-sterol-dependent signal pathway of LDL-Rs, by which endogenous cholesterol synthesis, that is, the [14C]acetate incorporation, is regulated through PKC activation.

Original languageEnglish
Pages (from-to)55-62
Number of pages8
JournalCell biochemistry and function
Volume25
Issue number1
DOIs
Publication statusPublished - Jan 1 2007

Keywords

  • Ca signal
  • Cholesterol synthesis
  • Human monocytes
  • Inositol trisphosphate
  • LDL-receptor
  • Protein kinase C

ASJC Scopus subject areas

  • Biochemistry
  • Clinical Biochemistry
  • Cell Biology

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