Inhibition of HgCl2-induced mitogen-activated protein kinase activation by LL-Z1640-2 in CCRF-CEM cells

Masato Matsuoka, Bambang Wispriyono, Yoshihisa Iryo, Hideki Igisu, Tsutomu Sugiura

Research output: Contribution to journalArticlepeer-review

12 Citations (Scopus)

Abstract

Exposure of HgCl2 to CCRF-CEM human lymphoblastoid cells induced phosphorylation of mitogen-activated protein kinases (MAPKs); extracellular signal-regulated protein kinase (ERK), c-Jun N-terminal kinase (JNK) and p38. LL-Z1640-2, a macrocyclic nonaketide, inhibited HgCl2-induced JNK phosphorylation at 5-100 ng/ml. It also inhibited phosphorylation of ERK and p38 but only at 100 ng/ml. The same doses of radicicol did not suppress MAPKs activation. LL-Z1640-2 (at 100 ng/ml) inhibited HgCl2-induced JNK phosphorylation in NIH 3T3 fibroblasts but not in LLC-PK1 renal epithelial cells. Thus, LL-Z1640-2 is a potent inhibitor of HgCl2-induced MAPKs activation, especially that of JNK, in CCRF-CEM cells. Copyright (C) 2000 Elsevier Science B.V.

Original languageEnglish
Pages (from-to)155-158
Number of pages4
JournalEuropean Journal of Pharmacology
Volume409
Issue number2
DOIs
Publication statusPublished - 8 Dec 2000

Keywords

  • HgCl
  • LL-Z1640-2
  • Mitogen-activated protein kinases
  • Radicicol
  • c-Jun N-terminal kinase

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